rss_2.0Archivum Immunologiae et Therapiae Experimentalis FeedSciendo RSS Feed for Archivum Immunologiae et Therapiae Experimentalishttps://sciendo.com/journal/AITEhttps://www.sciendo.comArchivum Immunologiae et Therapiae Experimentalis Feedhttps://sciendo-parsed.s3.eu-central-1.amazonaws.com/67521e2d8b676d152c20f24b/cover-image.jpghttps://sciendo.com/journal/AITE140216Antinuclear Antibodies in Non-Rheumatic Diseaseshttps://sciendo.com/article/10.2478/aite-2025-0004<abstract>
<title style='display:none'>Abstract</title>
<p>Antinuclear antibodies (ANAs) are critical immunological markers commonly associated with various connective tissue diseases (CTDs). However, these autoantibodies are also detectable in healthy individuals, patients with non-rheumatic autoimmune diseases, those with viral infections, and subjects using specific medications (such as procainamide, hydralazine, and minocycline) that can lead to drug-induced ANA elevation. The standard method for ANA detection is indirect immunofluorescence, a process that requires precision and thoroughness as it assesses both titer and fluorescence patterns. Additionally, immunoblotting and enzyme-linked immunosorbent assay (ELISA) are recommended to identify specific ANAs precisely, highlighting the importance of precision in ANA detection. This review explores the advantages and limitations of current ANA detection methods. It also describes the clinical implications of ANA presence in non-rheumatic diseases, including autoimmune disorders, infectious conditions, non-autoimmune and non-infectious diseases, and autoimmune cutaneous diseases. The presence of elevated ANA titers in these contexts can complicate clinical decision-making, as the diagnostic value of ANA testing alone is limited in non-rheumatic conditions. However, despite these limitations, ANA remains a key component in diagnosing and prognosis systemic CTDs, as it can indicate disease activity, severity, and response to treatment, which is of utmost importance in rheumatology and internal medicine. This paper provides a comprehensive review of the role of ANA in non-rheumatic diseases. It focuses on ANA diagnostic and prognostic significance and offers valuable insights for clinical practice.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2025-00042025-01-19T00:00:00.000+00:00CRISPR/Cas Systems as Diagnostic and Potential Therapeutic Tools for Enterohemorrhagic https://sciendo.com/article/10.2478/aite-2025-0003<abstract>
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<p>Following its discovery as an adaptive immune system in prokaryotes, the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated proteins (Cas) system has been developed into a multifaceted genome editing tool. This review compiles findings aimed at implementation of this technology for selective elimination or attenuation of enterohemorrhagic <italic>Escherichia coli</italic> (EHEC). EHEC are important zoonotic foodborne pathogens that cause hemorrhagic colitis and can progress to the life-threatening hemolytic uremic syndrome (HUS). Advancements in the application of CRISPR methodology include laboratory detection and identification of EHEC, genotyping, screening for pathogenic potential, and engineering probiotics to reduce microbial shedding by cattle, the primary source of human infection. Genetically engineered phages or conjugative plasmids have been designed to target and inactivate genes whose products are critical for EHEC virulence.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2025-00032025-01-07T00:00:00.000+00:00Quantification of Citrullinated Histone H3 as a Marker for Neutrophil Extracellular Traps Correlated to Clinical Characteristics of Patients with Systemic Lupus Erythematosushttps://sciendo.com/article/10.2478/aite-2025-0002<abstract>
<title style='display:none'>Abstract</title>
<p>Systemic lupus erythematosus (SLE) is an autoimmune disease whose pathogenesis is not fully understood to date. One of the suggested mechanisms for its development is NETosis, which involves the release of a specific network consisting of chromatin, proteins, and enzymes from neutrophils, stimulating the immune system. One of its markers is citrullinated histone H3 (H3Cit). This study aimed to evaluate the correlation of H3Cit levels with the clinical characteristics of 80 SLE patients. Levels of H3Cit in the subjects' serum were quantified spectrophotometrically. Statistical analysis was performed using MedCalc 15.8 and Statistica 13.3. Significantly higher H3Cit levels were found in patients with arthralgia (medians [interquartile range] [IQR]: 1.67 [1.67–1.69] <italic>vs</italic>. 1.67 [1.62–1.68], <italic>p</italic> = 0.0150, respectively) and reduced complement component C4 levels compared to patients without these conditions (medians [IQR]: 1.68 [1.67–1.70] <italic>vs</italic>. 1.68 [1.67–1.69], <italic>p</italic> = 0.0297, respectively). A significant weak negative correlation was observed between H3Cit levels and leukocytosis (rho = −0.2602, <italic>p</italic> = 0.0309) and reduced complement component C3 levels (rho = −0.2442, <italic>p</italic> = 0.0447) and a weak positive correlation with anti-double stranded DNA (anti-dsDNA) antibody levels (rho = 0.3794, <italic>p</italic> = 0.0036). Moreover, the clinical utility of the H3Cit assay in differentiating patients with arthralgia (area under the curve [AUC] = 0.709, <italic>p</italic> = 0.0115), seizures (AUC = 0.813, <italic>p</italic> = 0.0005), hepatomegaly (AUC = 0.746, <italic>p</italic> = 0.0111), and reduced levels of complement component C4 (AUC = 0.662, <italic>p</italic> = 0.0224) and without the above conditions was noted.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2025-00022025-01-03T00:00:00.000+00:00Unraveling the Complexity and Advancements of Transdifferentiation Technologies in the Biomedical Field and Their Potential Clinical Relevancehttps://sciendo.com/article/10.2478/aite-2025-0001<abstract>
<title style='display:none'>Abstract</title>
<p>Chronic diseases such as cancer, autoimmunity, and organ failure currently depend on conventional pharmaceutical treatment, which may cause detrimental side effects in the long term. In this regard, cell-based therapy has emerged as a suitable alternative for treating these chronic diseases. Transdifferentiation technologies have evolved as a suitable therapeutic alternative that converts one differentiated somatic cell into another phenotype by using transcription factors (TFs), small molecules, or small, single-stranded, non-coding RNA molecules (miRNA). The transdifferentiation techniques rely on simple, fast, standardized, and versatile protocols with minimal chance of tumorigenicity and genotoxicity. However, there are still challenges and limitations that need to be addressed to enhance their clinical translation percentage in the near future. Taking this into account, we have delineated the features and strategies used in the transdifferentiation techniques. Then, we delved into different intermediate states that were attained during transdifferentiation. Advancements in transdifferentiation techniques in the field of tissue engineering, autoimmunity, and cancer therapy were dissected. Furthermore, limitations, challenges, and future perspectives are outlined in this review to provide a whole new picture of the transdifferentiation techniques. Advancements in molecular biology, interdisciplinary research, bioinformatics, and artificial intelligence will push the frontiers of this technology further to establish new avenues for biomedical research.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2025-00012024-12-05T00:00:00.000+00:00Asymptomatic Hyperuricemia: A Nephro-Rheumatological Perspectivehttps://sciendo.com/article/10.2478/aite-2024-0024<abstract>
<title style='display:none'>Abstract</title>
<p>Hyperuricemia (HU) is a common disorder associated with gout, kidney injury, and high cardiovascular risk. However, whether high serum uric acid (sUA) is a causative factor or just comorbidity remains unclear. When asked if asymptomatic hyperuricemic patients need treatment, even artificial intelligence in the form of the GPT chat provides an ambivalent answer and refers us to a healthcare provider. We believe that such discrepancies stem from an incomplete understanding of the role that uric acid (UA) plays inside and outside the cell. With the rapid development of genomics, proteomics, immunology, and novel biomarkers, we are armed with new data to help us better understand the weight of inborn and environmental factors on an individual’s UA concentrations. This review sums up the latest progress that has been made in the field of asymptomatic HU, compares the results presented by various research teams, and indicates new directions that emerge for future studies.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00242024-11-29T00:00:00.000+00:00Polymorphic Variants in the Vitamin D Receptor and Clinical Parameters of Rheumatoid Arthritis Patients Undergoing Anti-TNF Treatmenthttps://sciendo.com/article/10.2478/aite-2024-0023<abstract>
<title style='display:none'>Abstract</title>
<p>Vitamin D levels have been related to the severity and progression of various autoimmune disorders. In this study, we aimed to investigate the impact of genetic variability in the vitamin D receptor (VDR) gene on disease susceptibility and progression in patients with rheumatoid arthritis (RA) treated with tumor necrosis factor (TNF) inhibitors. The study comprises 121 RA patients subjected to anti-TNF therapy genotyped for four VDR polymorphic variants: rs1544410 (<italic>Bsm</italic>I), rs2228570 (<italic>Fok</italic>I), rs731236 (<italic>Taq</italic>I), and rs7975232 (<italic>Apa</italic>I). There was no significant association between RA susceptibility and VDR genetic variants. The study results revealed that patients with the rs2228570 <italic>CC</italic> genotype were characterized by lower vitamin D3 levels (<italic>p</italic> = 0.028) than those with the <italic>T</italic> allele. Also, the vitamin D3 levels (<italic>p</italic> = 0.029) and age at diagnosis (<italic>p</italic> = 0.017) were significantly lower in rs7975232 <italic>A</italic> allele carriers compared to <italic>CC</italic> homozygotes. However, after 6 months of therapy, the <italic>A</italic> allele seemed to be related to lower disease activity score 28 (DAS28) values (<italic>p</italic> = 0.030) and more common in patients who achieved remission (<italic>p</italic> = 0.004) compared to the <italic>CC</italic> genotype. Concerning other investigated polymorphisms, patients carrying rs1544410 <italic>AA</italic> and rs731236 <italic>CC</italic> homozygosity had lower C-reactive protein (CRP) levels before therapy (<italic>p</italic> = 0.009). In conclusion, VDR rs2228570 and rs7975232 polymorphic variants were found to be related to vitamin D3 levels. Moreover, the genotyping of rs7975232 was also useful in evaluating disease onset and disease activity after 6 months of therapy with TNF inhibitors in RA patients.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00232024-11-10T00:00:00.000+00:00S-Adenosylmethionine Treatment Diminishes the Proliferation of Castration-Resistant Prostate Cancer Cells by Modulating the Expression of miRNAshttps://sciendo.com/article/10.2478/aite-2024-0022<abstract>
<title style='display:none'>Abstract</title>
<p>AdoMet (S-adenosylmethionine) inhibits cancer cell proliferation and migration via epigenetic alterations. This study aimed to investigate whether AdoMet may cause alterations in microRNA (miRNA) expression profiles that are important for the initiation and progression of prostate cancer. PC-3 cells were treated with AdoMet before miRNA sequencing. A total of 17 differentially expressed miRNAs were detected. Target gene prediction was performed by means of databases. Results were aligned to transcriptomic data. The bioinformatic analysis revealed upregulation of anticancerogenic genes, downregulation of cancerogenic-related processes and pathways. Knocking down hsa-miR-192-5p in PC-3 cells resulted in downregulation of cancer cell proliferation, thus confirming these results.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00222024-11-01T00:00:00.000+00:00Novel Insight into Inflammatory Pathways in Acute Pulmonary Embolism in Humanshttps://sciendo.com/article/10.2478/aite-2024-0021<abstract>
<title style='display:none'>Abstract</title>
<p>Accumulating data have shown a pathophysiological association between inflammatory pathways and thrombosis. Venous thromboembolism (VTE), which includes deep vein thrombosis (DVT) and acute pulmonary embolism (APE), is a significant health burden. It involves not only hemodynamic disturbances due to the emboli occluding the pulmonary arteries, but also platelet activation, endothelial dysfunction, and “firing up” of the inflammatory cascade. In humans, the systemic inflammatory state can also be evaluated using plasma levels of C-reactive protein (CRP) and interleukin (IL)-6, which correlate with venous obstruction, thrombus extension, and clinical VTE complications such as postthrombotic syndrome, recurrent thromboembolism, worse quality of life, and functional impairment. The exaggerated inflammatory state during postthrombotic syndrome aligns with severe alterations in endothelial function, such as activation of intercellular adhesion molecule (ICAM)-1 and E-selectin, as well as vascular proteolysis and fibrinolysis. Moreover, a hypercoagulable state, indicated by higher levels of von Willebrand factor (vWF) and factor VIII, is closely associated with the inflammatory response. We aimed to describe the role of basic inflammatory markers in daily clinical practice as well as the most important cytokines (IL-1β, IL-6, IL-8, tumor necrosis factor-a [TNF-α], growth differentiation factor-15 [GDF-15]). These markers could provide valuable insight into the interplay between thrombosis and inflammation, helping inform better management and treatment strategies.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00212024-10-28T00:00:00.000+00:00S-Adenosylmethionine Inhibits the Proliferation of Retinoblastoma Cell Y79, Induces Apoptosis and Cell Cycle Arrest of Y79 Cells by Inhibiting the Wnt2/β-Catenin Pathwayhttps://sciendo.com/article/10.2478/aite-2024-0020<abstract>
<title style='display:none'>Abstract</title>
<p>Retinoblastoma is one of the most common primary intraocular malignancies in young children. Traditional treatment methods such as chemotherapy often come with significant adverse effects, such as hearing loss, cognitive impairment, and vision loss. Therefore, there is an urgent need to explore a novel therapeutic drug that is both effective and safe. S-adenosylmethionine (SAM) is a natural compound known to exhibit anti-proliferative effects in various cancer cell lines. However, to date, no studies investigated the effects of SAM on retinoblastoma cells and its potential mechanisms of action. Therefore, this study aims to investigate the impact of SAM on retinoblastoma cells and explore its possible mechanisms of action, with the hope of providing new insights into the treatment of this disease. The optimal concentration of SAM was determined using the Cell Counting Kit-8 assay. The effect of SAM on retinoblastoma proliferation was assessed using the 5-ethynyl-2′-deoxyuridine cell proliferation assay. Y79 cells were subjected to hematoxylin and eosin stain and electron microscopy to observe any morphological changes induced by SAM. The stages of SAM’s action on the retinoblastoma cell cycle and its apoptotic effects were measured using flow cytometry. The apoptotic effect of SAM on retinoblastoma was further confirmed using the TUNEL assay. Differential expression of related genes was detected through RT-PCR. <italic>In vivo</italic> subcutaneous tumor formation in nude mice and immunohistochemistry were employed to validate the effect of SAM on retinoblastoma-related phenotypes. Western blotting was conducted to investigate whether SAM modulated retinoblastoma-related phenotypes via the Wnt2/β-catenin pathway. SAM arrested the cell cycle of retinoblastoma at the G1 phase, induced apoptosis of retinoblastoma cells through the Wnt2/β-catenin pathway, and affected their morphology and even ultrastructure. In addition, <italic>in vitro</italic> and <italic>in vivo</italic> experiments demonstrated that SAM had an oncogenic effect on retinoblastoma. In this study, we verify <italic>in vitro</italic> and <italic>in vivo</italic> whether SAM inhibits the proliferation of retinoblastoma cell Y7, induces apoptosis and cell cycle arrest of Y79 cells by inhibiting the Wnt2/β-catenin pathway, and affects the morphology and structure of retinoblastoma cell Y79.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00202024-10-04T00:00:00.000+00:00Apoptosis Regulation in Dental Pulp Cells and PD-1/PD-L1 Expression Dynamics Under Ozone Exposure – A Pilot Approachhttps://sciendo.com/article/10.2478/aite-2024-0019<abstract>
<title style='display:none'>Abstract</title>
<p>This study aimed to determine the effect of ozone on the expression of <italic>Bax</italic> and <italic>Bcl-2</italic> genes in dental pulp cells. Additionally, the programmed cell death protein 1, programmed death-ligand 1, and CD200 antigens were determined in lymphocytes to assess their surface expression. Dental pulp cells were cultured from extracted healthy third molars and characterized as dental pulp stromal cells. Gene expression of <italic>Bcl-2</italic> and <italic>Bax</italic> was analyzed at 0 s, 6 s, and 12 s of ozone exposure using real-time PCR. Lymphocytes from dental pulp were subjected to ozone exposure for 12 s and PD-1, PD-L1, and CD200/CD200R expression was analyzed by flow cytometry. Upon exposure to ozone for 6 s, the <italic>Bcl-2</italic> expression decreased significantly to −0.09, and at 12 s, it increased significantly to 0.3. <italic>Bax</italic> gene expression level increased significantly to 0.188 after 6 s exposure, and at 12 s, to 0.16. Lymphocytes exposed to ozone for 12 s showed minimal changes in PD-1, PD-L1, and CD200/CD200R expression levels, indicating that oxidative stress does not impact the signaling pathways regulating these molecules. The significant upregulation of <italic>Bcl-2</italic> at 12 s highlights the cells’ effort to protect themselves from prolonged oxidative stress, possibly tipping the balance toward cell survival and tissue repair. However, the absence of changes in PD-1 and PD-L1 expression on lymphocytes under oxidative stress suggests that these molecules are not sensitive to oxidative stress in this context.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00192024-09-14T00:00:00.000+00:00Endothelial Activation and Stress Index Score as a Prognostic Factor of Cytokine Release Syndrome in CAR-T Patients – A Retrospective Analysis of Multiple Myeloma and Large B-Cell Lymphoma Cohortshttps://sciendo.com/article/10.2478/aite-2024-0018<abstract>
<title style='display:none'>Abstract</title>
<p>Endothelial Activation and Stress Index (EASIX) has been proposed as a prognostic factor of adverse events or survival in hematological malignancies. Endothelial dysfunction has been associated with complications following stem cell transplantation and chimeric antigen receptor (CAR)-T therapy. This retrospective cohort study evaluated the utility of the EASIX score as a prognostic factor of cytokine release syndrome (CRS) in multiple myeloma/light-chain amyloidosis (MM/AL amyloidosis; N = 69) and large B-cell lymphoma (LBCL) cohorts (N = 65). Occurrence of CRS grade ≥3 was the primary endpoint. For both cohorts, the EASIX and simplified EASIX (s-EASIX) scores were calculated at four different time points before CAR-T infusion to assess its prognostic value. In the MM/AL amyloidosis cohort, neither EASIX nor s-EASIX scores calculated at any time point were associated with the occurrence of CRS grade ≥3. In the LBCL cohort, EASIX and s-EASIX scores measured before lymphodepletion (EASIX-pre and s-EASIX-pre) showed a significant relationship with CRS grade ≥3 (odds ratio [OR] = 1.06 and OR = 1.05, respectively). The cutoff value of 1.835 for EASIX-pre was associated with 4.59-fold increased OR of CRS grade ≥3 (95% confidence interval [CI]: 1.13–21.84), whereas s-EASIX-pre cutoff equaled 2.134 and was associated with 4.13-fold increased OR of CRS grade ≥3 (95% CI: 1.01–17.93). However, after internal validation with bootstrapping, the significance was lost both for the EASIX-pre and s-EASIX-pre cutoff. The presented findings indicate that the EASIX scores fail to predict CRS in MM/amyloidosis CAR-T patients, whereas they can be implemented as CRS grade ≥3 predictors in LBCL CAR-T patients.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00182024-09-14T00:00:00.000+00:00Angiotensin II Type 2 Receptor Antibodies in Glomerular Diseaseshttps://sciendo.com/article/10.2478/aite-2024-0017<abstract>
<title style='display:none'>Abstract</title>
<p>We evaluated the concentration of AT2R antibodies in 136 patients with primary and secondary glomerular diseases: membranous nephropathy (n = 18), focal and segmental glomerulosclerosis (n = 25), systemic lupus erythematosus (n = 17), immunoglobulin A (IgA) nephropathy (n = 14), mesangial (non-IgA) proliferative nephropathy (n = 6), c-ANCA vasculitis (n = 40), perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA) vasculitis (n = 16), and compared it with a healthy control group (22 patients). Serum creatinine levels, proteinuria, serum albumin, and total protein concentrations were prospectively recorded for 2 years. The mean levels of AT2R antibodies in the lupus nephropathy group were significantly higher compared to the control group, 64.12 ± 26.95 units/mL and 9.72 ± 11.88 units/mL, respectively. There was no association between this level and the clinical course of the disease. The AT2R levels in other kinds of glomerular disease were no different from the control group. We found significant correlations between AT1R and AT2R in patients with membranous nephropathy (r = 0.66), IgA nephropathy (r = 0.61), and c-ANCA vasculitis (r = 0.63). Levels of AT2R antibodies in systemic lupus erythematosus are higher compared to other types of glomerulonephritis, vasculitis, and a healthy control group. Levels of AT2R antibodies correlate with AT1R antibodies in the groups of patients with membranous nephropathy, IgA nephropathy, and c-ANCA vasculitis. These kinds of AT2R antibodies have a stimulative effect on AT2R, but we have not found the influence of these antibodies on the clinical course of glomerular diseases.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00172024-08-19T00:00:00.000+00:00The Healthcare Study Examines the Humoral Anti-S1 Antibody Response Following mRNA Vaccination, Comparing Individuals with and without Prior SARS-CoV-2 Infectionhttps://sciendo.com/article/10.2478/aite-2024-0016<abstract>
<title style='display:none'>Abstract</title>
<p>Vaccines targeting severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been pivotal in curtailing the spread of infection. Health care workers, as frontline responders, were among the first to receive vaccination to mitigate coronavirus disease in 2019 (COVID-19) transmission. This study aimed to assess the humoral response elicited by mRNA vaccines, specifically measuring antibodies against the spike S1 protein, a marker of immune response. A cohort of 649 health care workers received three doses of mRNA vaccine, with antibody levels evaluated before and after each dose within a 2- to 3-week interval. Participants were stratified into groups based on prior exposure to the virus: those without prior contact (440 individuals) and those with a history of infection (209 individuals). Among the latter, cases of SARS-CoV-2 infection ranged from asymptomatic (92 individuals) to mild symptomatic (117 individuals). Participants with a history of infection exhibited elevated levels of IgG antibodies against the S1 protein prior to vaccination. Notably, both immunoglobulin IgA class (IgA) and immunoglobulin IgG class (IgG) antibody responses increased significantly post-vaccination, peaking after the second dose for IgG and after the third dose for IgA. Interestingly, the immune response to the vaccine did not vary significantly based on the symptomatic or asymptomatic nature of prior infection. Furthermore, the study findings indicate that completion of the vaccination regimen led to sustained antibody production lasting between 6 months and 9 months. This study underscores the robust and enduring humoral response elicited by mRNA vaccines, particularly among health care workers, irrespective of prior SARS-CoV-2 exposure.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00162024-08-15T00:00:00.000+00:00Clinical Significance of IgG4 Serum Concentration in Graves’ Diseasehttps://sciendo.com/article/10.2478/aite-2024-0015<abstract>
<title style='display:none'>Abstract</title>
<p>Elevated immunoglobulin G4 (IgG4) serum antibodies are an important feature of IgG4-related disease. However, IgG4 antibodies can play a role in autoimmune thyroid disorders. In this study, we aimed to evaluate the impact of serum IgG4 levels on clinical features of Graves’ disease (GD). We recruited 60 patients with GD (48 patients without thyroid eye disease, 12 patients with moderate-to-severe Graves’ orbitopathy [GO], and 25 healthy control subjects). The prevalence of high IgG4 serum concentration was 4.2% among GD patients without GO and 33.33% in patients with moderate-to-severe GO. The group with GO had significantly higher median IgG4 levels (87.9 mg/dL) than the control group (41.2 mg/dL, <italic>P</italic> = 0.034) and the GD without GO group (30.75 mg/dL, <italic>P</italic> < 0.001). Patients with thyroid nodules had lower IgG4 levels than patients without thyroid nodules, but the difference was not statistically significant (35.7 [24.8; 41.53] mg/dL vs. 43 [30.1; 92.7] mg/dL, <italic>P</italic> = 0.064). IgG4 as a diagnostic tool for moderate-to-severe GO had the following parameters: area under the curve (AUC): 0.851 (<italic>P</italic> < 0.001), at the cut-off value of 49 mg/dL, negative predictive value: 100%, positive predictive value: 48%, sensitivity: 100%, specificity: 73%. There were no significant differences between the high and normal IgG4 groups in thyroid hormones, antithyroid antibodies, and ultrasound features. Serum IgG4 levels are associated with some of the clinical features of GD and can help in the diagnostic process of the disease. More research is needed to better understand the pathophysiology of IgG4 involvement in GD.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00152024-07-20T00:00:00.000+00:00Solute Carrier Transporters in Synovial Membrane and Hoffa’s Pad of Patients with Rheumatoid Arthritishttps://sciendo.com/article/10.2478/aite-2024-0014<abstract>
<title style='display:none'>Abstract</title>
<p>Rheumatoid arthritis (RA) is a complex autoimmune disease that leads to joint destruction. A number of immune cells that affect joint tissues are involved in the pathogenesis of this disease. This leads to the synthesis of many pro-inflammatory mediators. The transport of drugs, as well as many cytokines involved in the development of inflammation in RA patients, is mediated by membrane transporters. Membrane transporters are proteins that mediate the transfer of substrates across biological membranes. But to date there are no studies examining the expression of solute carrier (SLC) transporters in joint tissues. The aim of the study was to evaluate the expression of individual SLC family transporters in the synovial membranes (SMs) and infrapatellar fat pad (Hoffa’s pad) of RA patients. The study included 20 patients with rheumatoid arthritis and 20 with osteoarthritis as the control group who were undergoing joint replacement surgery as a normal part of clinical care. In the SM and Hoffa’s pad of RA patients the following 17 membrane transporters were defined at relevant expression levels for SLC transporter superfamily: <italic>SLC15A2, SLC16A3, SLC19A1, SLC2A9, SLC22A1, SLC22A3, SLC22A4, SLC22A5, SLC22A18, SLC33A1, SLC47A1, SLC51A, SLC7A5, SLC7A6, SLC01C1, SLC02B1, SLC04A1</italic>. The confirmed expression of these transporters in the SMs as well as Hoffa’s pad of patients with RA and OA, and the differences in their expression between these groups, suggests the involvement of SLC transporters in both the maintenance of homeostasis under physiological conditions in the tissues of the joints, as well as in the inflammatory process in RA.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00142024-06-27T00:00:00.000+00:00The Pathogenesis of Foot-and-Mouth Disease Virus Infection: How the Virus Escapes from Immune Recognition and Eliminationhttps://sciendo.com/article/10.2478/aite-2024-0013<abstract>
<title style='display:none'>Abstract</title>
<p>Foot-and-mouth disease virus (FMDV) is a highly contagious and economically devastating pathogen that affects cloven-hoofed animals worldwide. FMDV infection causes vesicular lesions in the mouth, feet, and mammary glands, as well as severe systemic symptoms such as fever, salivation, and lameness. The pathogenesis of FMDV infection involves complex interactions between the virus and the host immune system, which determine the outcome of the disease. FMDV has evolved several strategies to evade immune recognition and elimination, such as antigenic variation, receptor switching, immune suppression, and subversion of innate and adaptive responses. This review paper summarizes the current knowledge on the pathogenesis of FMDV infection and the mechanisms of immune evasion employed by the virus. It also discusses the challenges and opportunities for developing effective vaccines and therapeutics against this important animal disease.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00132024-06-24T00:00:00.000+00:00MICB Genetic Variants and Its Protein Soluble Level Are Associated with the Risk of Chronic GvHD and CMV Infection after Allogeneic HSCThttps://sciendo.com/article/10.2478/aite-2024-0012<abstract>
<title style='display:none'>Abstract</title>
<p>The aim of the present study was to determine the associations between the <italic>MICB</italic> genetic variability and the expression and the risk of development of post-transplant complications after allogeneic hematopoietic stem cell transplantation (HSCT). HSCT recipients and their donors were genotyped for two <italic>MICB</italic> polymorphisms (rs1065075, rs3828903). Moreover, the expression of a soluble form of MICB was determined in the recipients' serum samples after transplantation using the Luminex assay. Our results revealed a favorable role of the <italic>MICB</italic> rs1065075 <italic>G</italic> allele. Recipients with donors carrying this genetic variant were less prone to developing chronic graft-versus-host disease (cGvHD) when compared to recipients without any symptoms of this disease (41.41% <italic>vs.</italic> 65.38%, <italic>p</italic> = 0.046). Moreover, the <italic>MICB</italic> rs1065075 <italic>G</italic> allele was associated with a lower incidence of cytomegalovirus (CMV) reactivation, both as a donor (<italic>p</italic> = 0.015) and as a recipient allele (<italic>p</italic> = 0.039). The <italic>MICB</italic> rs1065075 <italic>G</italic> variant was also found to be associated with decreased serum soluble MICB (sMICB) levels, whereas serum sMICB levels were significantly higher in recipients diagnosed with CMV infection (<italic>p</italic> = 0.0386) and cGvHD (<italic>p</italic> = 0.0008) compared to recipients without those complications. A protective role of the <italic>G</italic> allele was also observed for the rs3828903 polymorphism, as it was more frequently detected among donors of recipients without cGvHD (89.90% <italic>vs.</italic> 69.23%; <italic>p</italic> = 0.013). <italic>MICB</italic> genetic variants, as well as serum levels of sMICB, may serve as prognostic factors for the risk of developing cGvHD and CMV infection after allogeneic HSCT.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00122024-06-07T00:00:00.000+00:00Abnormalities of Coagulation and Fibrinolysis Assessed by Thromboelastometry in an Endotoxic Shock Model in Piglets Treated with Nitric Oxide and Hydrocortisonehttps://sciendo.com/article/10.2478/aite-2024-0011<abstract>
<title style='display:none'>Abstract</title>
<p>This is an animal model study to investigate changes in hemostasis during endotoxemic shock and to determine whether the combination of inhaled nitric oxide (iNO) + intravenous hydrocortisone had an effect on clot formation and fibrinolysis. iNO selectively decreases pulmonary artery pressure, without affecting cardiac index or systemic vascular resistance; however, the results of studies on the possible consequences of iNO administration on coagulation are inconsistent and require further research. Thirty-four piglets were included. Administering endotoxin caused severe hypodynamic shock. Half of the animals received iNO (30 ppm) + hydrocortisone, starting 3 h after endotoxin infusion and continuing to the end of the study. All animals developed coagulation disorders, manifested by a tendency to hypocoagulation; at the same time, fibrinolysis was impaired. Coagulation and fibrinolysis disorders persisted after endotoxin infusion was discontinued, with worse severity in the animals that died before the study was terminated. Administering iNO + hydrocortisone did not cause further changes in coagulation and fibrinolysis parameters, either during or after the endotoxin challenge, suggesting that potential therapeutic interventions with iNO to lower pulmonary arterial pressure will not affect hemostasis.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00112024-06-07T00:00:00.000+00:00Transplantation of Donor–Recipient Chimeric Cells Restores Peripheral Blood Cell Populations and Increases Survival after Total Body Irradiation-Induced Injury in a Rat Experimental Modelhttps://sciendo.com/article/10.2478/aite-2024-0009<abstract>
<title style='display:none'>Abstract</title>
<p>Current therapies for acute radiation syndrome (ARS) involve bone marrow transplantation (BMT), leading to graft-versus-host disease (GvHD). To address this challenge, we have developed a novel donor–recipient chimeric cell (DRCC) therapy to increase survival and prevent GvHD following total body irradiation (TBI)-induced hematopoietic injury without the need for immunosuppression. In this study, 20 Lewis rats were exposed to 7 Gy TBI to induce ARS, and we assessed the efficacy of various cellular therapies following systemic intraosseous administration. Twenty Lewis rats were randomly divided into four experimental groups (<italic>n</italic> = 5/group): saline control, allogeneic bone marrow transplantation (alloBMT), DRCC, and alloBMT + DRCC. DRCC were created by polyethylene glycol-mediated fusion of bone marrow cells from 24 ACI (RT1a) and 24 Lewis (RT11) rat donors. Fusion feasibility was confirmed by flow cytometry and confocal microscopy. The impact of different therapies on post-irradiation peripheral blood cell recovery was evaluated through complete blood count, while GvHD signs were monitored clinically and histopathologically. The chimeric state of DRCC was confirmed. Post-alloBMT mortality was 60%, whereas DRCC and alloBMT + DRCC therapies achieved 100% survival. DRCC therapy also led to the highest white blood cell counts and minimal GvHD changes in kidney and skin samples, in contrast to alloBMT treatment. In this study, transplantation of DRCC promoted the recovery of peripheral blood cell populations after TBI without the development of GVHD. This study introduces a novel and promising DRCC-based bridging therapy for treating ARS and extending survival without GvHD.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00092024-05-23T00:00:00.000+00:00Dendritic Cells and the Establishment of Fetomaternal Tolerance for Successful Human Pregnancyhttps://sciendo.com/article/10.2478/aite-2024-0010<abstract>
<title style='display:none'>Abstract</title>
<p>Pregnancy is a remarkable event where the semi-allogeneic fetus develops in the mother’s uterus, despite genetic and immunological differences. The antigen handling and processing at the maternal–fetal interface during pregnancy appear to be crucial for the adaptation of the maternal immune system and for tolerance to the developing fetus and placenta. Maternal antigen-presenting cells (APCs), such as macrophages (Mφs) and dendritic cells (DCs), are present at the maternal–fetal interface throughout pregnancy and are believed to play a crucial role in this process. Despite numerous studies focusing on the significance of Mφs, there is limited knowledge regarding the contribution of DCs in fetomaternal tolerance during pregnancy, making it a relatively new and growing field of research. This review focuses on how the behavior of DCs at the maternal–fetal interface adapts to pregnancy’s unique demands. Moreover, it discusses how DCs interact with other cells in the decidual leukocyte network to regulate uterine and placental homeostasis and the local maternal immune responses to the fetus. The review particularly examines the different cell lineages of DCs with specific surface markers, which have not been critically reviewed in previous publications. Additionally, it emphasizes the impact that even minor disruptions in DC functions can have on pregnancy-related complications and proposes further research into the potential therapeutic benefits of targeting DCs to manage these complications.</p>
</abstract>ARTICLEtruehttps://sciendo.com/article/10.2478/aite-2024-00102024-05-23T00:00:00.000+00:00en-us-1