IntroductionHaploinsufficiency of A20 (HA20) is a monogenic disease caused by heterozygous TNFAIP3 variants. Despite the marked clinical variability, no genotype–phenotype correlation or validated laboratory biomarkers have been identified so far. Neurobehavioural abnormalities have been reported in murine models, but their prevalence in humans remains unclear.ObjectivesTo describe a cohort of patients with HA20 from two centres, evaluating age-related clinical variability; to assess the prevalence of neuropsychiatric symptoms; to explore the inflammatory profile of the patients, including interferon (IFN)-γ-inducible chemokines (CXCL9/10) and type 1 IFN signature (IS), as well as the therapies administered.MethodsClinical and laboratory data of 17 subjects from six families heterozygous for TNFAIP3 variants (American College of Medical Genetics and Genomics class 4–5) were retrospectively collected. Disease activity, treatments, CXCL9/10 and IS levels were collected. Continuous variables were expressed as medians (IQR). Age at onset was compared using the Kruskal-Wallis test, and groups were compared through the Wilcoxon test or Fisher’s exact test.ResultsClinical manifestations included oral aphthosis (88%), recurrent fever (53%), gastrointestinal inflammation (53%), autoimmunity (47%), genital ulcers (47%), neuropsychiatric symptoms (41%), arthritis/tenosynovitis (18%) and skin inflammation (12%). Disease onset before 5 years of age was associated with a higher prevalence of neuropsychiatric symptoms during lifetime (p=0.004), whereas arthritis was more common in patients with later onset. The median age at onset differed significantly according to the type of clinical manifestation (p<0.001). Higher IS levels were found in patients with active disease (p<0.01).ConclusionsHA20 shows marked clinical heterogeneity both between and within families. Clinical manifestations appear age-related and early disease onset was associated with increased neuropsychiatric involvement lifetime. Finally, type 1 IS may represent a potential biomarker of disease activity in HA20.

Elevated CD71 Expression on CD4⁺ T Cells in Egyptian SLE Patients: A Potential Biomarker for Disease Activity and Renal Involvement

Systemic lupus erythematosus (SLE) is a prototypical autoimmune disease in which host-microbiota crosstalk plays a pivotal role in immune dysregulation. Recent metagenomic studies have revealed that disease-specific dysbiosis--characterized by the expansion of pathobionts and depletion of immunoregulatory commensals--occurs across the gut, oral cavity, skin, and genital tract. Integrative multi-omics analyses have identified three mechanistic pathways linking microbial imbalance to autoimmunity: (1) microbial peptides trigger molecular mimicry and epitope spreading, activating autoreactive lymphocytes: (2) microbial metabolites disrupt redox homeostasis, impair epithelial barriers, and skew the AhR-mediated Th17/Treg balance; and (3) dysbiosis alters epigenetic regulation by inhibiting DNA methyltransferases, leading to hypomethylation of SLE-risk genes. Translational studies have shown that microbiome-targeted interventions, including probiotics, prebiotics, fecal microbiota transplantation, and even B cell-depleting chimeric antigen receptor T-cell (CAR-T) therapy, can restore microbial balance, reduce autoantibody levels, and modulate the gut-immune axis. Furthermore, microbial signatures are emerging as potential biomarkers for disease activity and treatment response. Despite this promise, challenges remain, such as the impact of immunosuppressants on the microbiota, spatial heterogeneity in host-microbe interactions, and limitations in causal inference. Looking forward, integrating single-cell metagenomics, microbiota-directed diets, and engineered microbial consortia may pave the way for personalized microbiome-based therapies. Reframing SLE as a "meta-organismal imbalance" positions microbial ecology at the forefront of precision medicine.

Telitacicept, a novel fusion protein that targets B lymphocyte stimulator and a proliferation-inducing ligand, has been used in autoimmune diseases. However, the efficacy and safety of telitacicept combined with glucocorticoids (GCs) in the treatment of immunoglobulin A nephropathy (IgAN) remain unclear. We recruited a total of 71 IgAN patients who received telitacicept without concurrent immunosuppressive therapy. Among them, 40 patients who received telitacicept 160 mg weekly and had not received GCs within the previous 3 months were further analyzed. Patients treated with telitacicept alone formed the telitacicept-alone subgroup, while those who received telitacicept plus GCs formed the telitacicept + GC subgroup. The primary outcome was the change in 24-h proteinuria from baseline over time. The telitacicept + GC subgroup showed a greater reduction in mean proteinuria (-84.1%, IQR: -90.4% to -74.4%) compared with the telitacicept-alone subgroup (-71.4%, IQR: -88.5% to -33.5%; p = 0.043) at 6 months. The eGFR slightly increased with no significant difference (8.8% vs. 8.1%; p = 0.91). Both groups showed reductions in serum IgA, IgG levels, and the percentage of patients with hematuria. Urinary soluble CD163, a potential biomarker of disease activity, also significantly decreased following telitacicept treatment (-4.33 ng/mg; p = 0.001). No serious adverse events were reported. In conclusion, telitacicept combined with glucocorticoids may offer a greater reduction in proteinuria than telitacicept monotherapy in IgAN patients, with preserved renal function. These findings support potential benefit of adjunctive GC therapy in selected patients undergoing telitacicept treatment.

Immune-mediated necrotizing myopathy (IMNM) is a severe autoimmune myopathy causing proximal muscle weakness. Its underlying immunopathogenesis remains incompletely understood, limiting the development of targeted therapies. To elucidate disease mechanisms and inform therapeutic strategies, this study characterized the peripheral immune profile of treatment-naïve IMNM patients. This retrospective study analyzed serum cytokine levels, complement proteins (C3, C4), immunoglobulins (IgA, IgG, and IgM), and peripheral blood lymphocyte subsets in 28 treatment-naïve IMNM patients during the active disease phase and 25 healthy controls at Tongji Hospital from August 2023 to March 2025. Compared with healthy controls, IMNM patients showed significantly elevated serum concentrations of interleukin-6 and interferon-γ (both p < 0.001). IgG and IgM levels were also markedly higher in the IMNM group (p = 0.003; p = 0.002). The number and percentage of B cells were significantly increased in IMNM patients (both p = 0.004). The number and percentage of CD8+ T cells were similarly elevated (p = 0.009; p = 0.004). In contrast, the proportion of CD4+ T cells was significantly reduced (p = 0.002), and the absolute count of natural killer cells was also significantly reduced (p = 0.004). IMNM exhibits a distinct peripheral immune landscape, characterized by enhanced humoral immunity potentially driven by CD8+ T cell-mediated mechanisms, accompanied by reduced circulating natural killer cells. These findings suggest potential biomarkers for disease activity and may inform targeted immunotherapies. Further studies are needed to validate these immune alterations and clarify their role in IMNM pathogenesis.

This study aimed to determine whether interferon regulatory factor 5 (IRF5) activation and its temporal dynamics in immune cells correlate with disease activity and flares in patients with systemic lupus erythematosus (SLE). Patients with SLE were prospectively enrolled and followed up for 52 weeks. The IRF5 nuclear translocation rate (NTR) was assessed in monocytes, dendritic cells, and B cells during baseline and follow-ups. Associations among IRF5 NTR, disease activity, and flares were statistically analyzed. Of 40 patients enrolled, 27 were included in the analysis after meeting all inclusion criteria. Baseline IRF5 NTR in B cells was correlated with SLE disease activity index scores (r = 0.529, p = 0.005). Nineteen patients developed flares, and high baseline IRF5 NTR showed good predictive accuracy (AUC = 0.763) and an increased flare risk (OR = 25.5, p = 0.003). In survival analysis, patients with high IRF5 NTR had significantly shorter flare-free survival (log-rank p = 0.030) and higher hazard of flare (HR = 7.43, p = 0.010). IRF5 NTR further increased during the 12 weeks preceding flares (p = 0.040). The IRF5 NTR in B cells is a potential biomarker for disease activity and flare prediction in SLE.

Background and Objectives: Reliable laboratory markers that accurately reflect disease activity in ankylosing spondylitis (AS) are limited. Conventional acute-phase reactants do not consistently correlate with clinical activity. Composite hematological indices derived from complete blood count may better capture systemic inflammatory burden. In this study, we aimed to investigate hematologic parameters in AS and to assess their relationships with disease activity. Materials and Methods: This retrospective observational study included 196 patients with AS. Disease activity was defined as a Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) ≥4. Demographic variables, laboratory parameters, hematological indices, and extra-articular manifestations were evaluated. Variable selection was performed using least absolute shrinkage and selection operator (LASSO) regression with ten-fold cross-validation. Variables with non-zero coefficients were entered into a multivariable logistic regression model. Model performance was assessed using receiver operating characteristic (ROC) curve analysis. Results: Ninety-seven (49%) patients had active disease. LASSO regression identified erythrocyte sedimentation rate (ESR), white blood cell count, red cell distribution width (RDW), platelet-to-lymphocyte ratio (PLR), and selected extra-articular manifestations as relevant predictors. In multivariable logistic regression, ESR (OR 1.03, 95% CI 1.00-1.06), white blood cell count (OR 1.23, 95% CI 1.04-1.46), and PLR (OR 1.01, 95% CI 1.003-1.020) were independently associated with active disease, while RDW showed a borderline association. The model demonstrated good discriminative ability (AUC 0.77, 95% CI 0.69-0.84). Conclusions: PLR is independently associated with disease activity in ankylosing spondylitis and improves discrimination when incorporated into a multivariable model. Easily accessible hematological indices may complement traditional inflammatory markers in the assessment of disease activity in routine clinical practice.

HLA-B27 positivity is strongly associated with acute anterior uveitis (AAU). This study investigated HLA-B27-dependent metabolic alterations in AAU and identified potential biomarkers of disease activity using plasma metabolomics. Untargeted and targeted metabolomics were employed to compare plasma metabolic profiles of HLA-B27-positive and negative patients. Distinct metabolic signatures, characterised by significant alterations in pyruvic acid and L-kynurenine, were identified in HLA-B27-positive individuals compared to HLA-B27-negative individuals. Furthermore, citric acid levels in these HLA-B27-positive patients correlated significantly with disease activity, particularly in those not receiving systemic medication. Pathway analysis revealed significant differences between HLA-B27-positive and negative patients in several key metabolic pathways, including the citrate cycle, tryptophan metabolism, pyruvate metabolism, and glycolysis/gluconeogenesis. A diagnostic model with citric acid alongside C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) demonstrated improved performance in predicting disease activity compared to a model utilising CRP and ESR alone (AUC: 0.727 vs. 0.713 and 0.674 vs. 0.670 in the untargeted and targeted cohorts, respectively). These findings offer insights into the metabolic dysregulation associated with HLA-B27-positive AAU and suggest that citric acid may be a potential biomarker for assessing disease activity, warranting further validation.

Rheumatoid arthritis (RA) is a chronic, multifactorial autoimmune disease characterized by symmetrical polyarthritis, joint pain, and swelling, which can lead to disability and premature death. Increasing attention has focused on epigenetic mechanisms, including non-coding RNAs in circular and linear forms, in RA pathogenesis. This study aimed to identify novel supportive RNA-based biomarkers associated with RA disease activity. The discovery cohort included 18 RA patients and 10 healthy controls (HCs). Peripheral blood mononuclear cells were analyzed using targeted RNA sequencing, encompassing both linear (LINOUT) and circular (CIRC) RNA forms, to assess differences between RA patients and HCs, as well as between high (HDA; DAS28 > 5.1; n = 10) and low disease activity/remission (LDA/REM; DAS28 ≤ 3.2; n = 8) disease activity groups. The results were validated in cohort of 45 patients with RA, divided into a high disease activity group (HDA; DAS28 > 5.1; n = 22) and a non-high disease activity group (non-HDA; DAS28 ≤ 5.1; n = 23) along with 24 control subjects, using quantitative PCR (qPCR). LMTK2 LINOUT expression correlated negatively with disease activity = -0.30) and distinguished RF-negative patients (n = 17) from HCs (p = 0.027). Expression was significantly lower in the high activity group (n = 22) versus the non-high activity group (n = 23; p = 0.022). Post-hoc ANOVA showed significant differences among HDA, non-HDA, and HCs (p = 0.001), with reduced expression in HDA versus non-HDA (p = 0.038) and increased expression in non-HDA versus controls (p = 0.001). EML6 LINOUT expression exhibited activity-dependent changes (p = 0.034) and positively correlated with disease activity = 0.303). Integration with erythrocyte sedimentation rate (ESR) improved discriminative performance. Combining LMTK2 LINOUT + EML6 LINOUT + ESR yielded the highest accuracy (AUC = 0.923). LMTK2 and EML6 show disease activity-dependent expression in RA and provide complementary information to conventional inflammatory parameters such as ESR. Their integration may improve diagnostic performance, highlighting their potential as novel supportive molecular biomarkers in RA.

The present study investigated the relationship between serum Matrix metalloproteinase-3 (MMP3) levels in Primary Sjögren's syndrome (pSS) patients and disease activity, clinical parameters, and different clinical manifestations of pSS. Serum samples were obtained from 77 pSS patients and 77 healthy controls (HC). MMP3 levels were detected using a biochemical analyzer. Disease activity was assessed using the Sjögren's Syndrome Disease Activity Index (SSDAI) and the EULAR Sjögren's Syndrome Disease Activity Index (ESSDAI). Pearson correlation analysis was employed to evaluate the relationship between MMP3 levels and clinical parameters. Serum MMP3 levels in pSS patients were significantly elevated compared to HC (P < 0.0001). Serum MMP3 levels were significantly positively correlated with WBC counts (r = 0.564, P < 0.0001), neutrophil counts (r = 0.5225, P < 0.0001), and serum LDH levels (r = 0.459, P < 0.0001). Moreover, MMP3 levels were significantly positively correlated with both SSDAI scores (r = 0.407, P = 0.002) and ESSDAI scores (r = 0.3061, P = 0.0068). Serum MMP3 levels are significantly elevated in pSS patients and show significant positive correlations with both SSDAI and ESSDAI scores, as well as key inflammatory parameters (WBC, neutrophil counts, LDH). In conclusion, these consistent associations suggest the potential of serum MMP3 as a biomarker for tracking disease activity in pSS. Key Points • Serum MMP3 levels were significantly elevated in pSS patients. • Serum MMP3 levels showed strong associations with disease activity, WBC counts and neutrophil counts. • MMP3 may serve as a biomarker for tracking pSS activity.

To assess the relation between the proportion of myeloid-derived suppressor cells (MDSCs), monocyte subsets, and the clinical phenotypes and disease activity of psoriatic disease (PsD), including psoriasis (PsO) and PsA. We carried out a cross-sectional study including 47 patients with PsD and 10 age- and sex-paired healthy controls. Using multiparametric flow cytometry, we evaluated the granulocytic (G) and monocytic (M) MDSCs, classical, intermediate and non-classical monocytes in peripheral blood. We compared these cell populations according to the clinical features, phenotype of PsD, and treatment groups. We evaluated their capability to predict disease activity measured by Psoriasis Area and Severity Index (PASI) and Disease Activity in Psoriatic Arthritis (DAPSA) by multivariate logistic and linear regressions. In comparison with healthy donors, PsD patients displayed lower mature G-MDSCs (5.88% vs 60.97%), increased M-MDSCs (0.62% vs 0.02%), decreased expression of arginase-1 and Programmed death-ligand 1 (PDL1), and expansion of non-classical monocytes (12.2% vs 4.68%). Increased mature G-MDSCs and decreased arginase-1 expression were seen in patients with cutaneous features. G-MDSCs were associated with cutaneous disease activity [PASI (β = 5.05, P = 0.05)], whilst non-classical monocytes were related to active PsA [DAPSA (β = 0.68, P = 0.004)], highlighting their potential as disease activity biomarkers. In PsD, G-MDSCs relate to cutaneous disease activity, whereas non-classical monocytes correlate with musculoskeletal features, highlighting their role as potential biomarkers of disease activity in PsD. Further prospective studies addressing the function of these cell subtypes would confirm their relationship with PsD activity status.

Lupus nephritis (LN) can affect up to 60% of patients with systemic lupus erythematosus (SLE). The NLRP3 inflammasome has been implicated in the pathogenesis of LN. This study aimed to evaluate the role of the NLRP3 inflammasome as a predictor of response to immunosuppressive treatment in patients with active LN. A prospective cohort study was conducted with 20 adult patients with active LN, classes III, IV, and V, from January 2021 to September 2023. Patients were followed up at biopsy (T0) and 6 months (T6) and 12 months (T12) after treatment and classified according to the primary efficacy renal response (PERR) at 12 months. Gene expression of NLRP3, CARD8, CASP1, IL1B, and IL18 was evaluated by RT-qPCR in PBMCs. Immunohistochemistry (IHC) for NLRP3 was performed on kidney tissue. The concentration of cytokine IL-1β was measured using the BD™ Cytometric Bead Array (CBA). The mean age was 31.9 ± 8.3 years, with 19 females and 1 male. After 12 months, 65% of patients achieved PERR. The IHC intensity in inflammatory cells was higher in patients with no PERR (p = 0.0426). In the no-PERR group, the gene expression of IL1B showed a significant increase at T6 (FC = 2.22: p = 0.0037) and T12 (FC = 2.91; p = 0.0001) compared with T0. Relative expression of IL1B was higher in no-PERR patients at T12 compared to the PERR group (p = 0.0477). The no-PERR group also had higher serum IL-1β levels compared to the PERR group at 12 months (2.9 ± 0.5 vs. 2.5 ± 0.7, p = 0.0164). In conclusion, our study evidenced an increase in IL1B expression and IL-1β levels over the 12 months of treatment in no-PERR patients, suggesting a potential biomarker of disease activity. Furthermore, a strong NLRP3 IHC staining score was associated with a higher likelihood of no PERR, highlighting the potential of the NLRP3 inflammasome as a predictor of worse clinical outcomes.

BackgroundNon–cystic fibrosis bronchiectasis (NCFB) is a chronic respiratory condition characterized by irreversible bronchial dilatation and persistent inflammation. Although inflammation plays a central role in disease progression, the upstream regulatory mechanisms remain incompletely understood. MicroRNA-155 (miR-155) is a well-recognized modulator of immune responses in chronic lung diseases, but its role in NCFB has not been previously elucidated.MethodsThis study enrolled 58 NCFB patients and 30 healthy controls. The expression of miR-155 in peripheral blood mononuclear cells (PBMC) was quantified using qRT-PCR. Serum levels of IL-1β, IL-6, IL-8, and TNF-α were assessed by ELISA. Correlations between miR-155 expression and inflammatory cytokines, clinical indices, and Pseudomonas aeruginosa colonization were evaluated. In vitro, BEAS-2B epithelial cells were transfected with miR-155 mimics or inhibitors, and cytokine production was measured following LPS stimulation.ResultsMiR-155 expression was significantly elevated in NCFB patients and positively correlated with IL-6, IL-8, TNF-α, and IL-1β levels (all p < 0.01). Higher miR-155 expression was also associated with increased disease burden, including elevated BSI scores and P. aeruginosa colonization. In vitro, miR-155 overexpression in BEAS-2B cells markedly enhanced pro-inflammatory cytokine secretion upon LPS stimulation, while inhibition of miR-155 suppressed cytokine release.ConclusionmiR-155 is upregulated in NCFB and closely associated with systemic and airway inflammation. It actively promotes pro-inflammatory signaling in airway epithelial cells, suggesting a pathogenic role in sustaining chronic inflammation. These findings highlight miR-155 as a potential biomarker of disease activity and a candidate target for immune modulation in bronchiectasis.

Immunological heterogeneity in Ménière's disease: CD4+ T cell subset profiling reveals three distinct Immunophenotypes.

Background and Objectives: Multiple myeloma (MM) remains an incurable plasma cell malignancy with heterogeneous clinical outcomes. Although current prognostic systems integrate biochemical and cytogenetic parameters, they do not fully capture disease complexity. Adipocytes within the bone marrow microenvironment secrete adipokines that regulate inflammation, metabolism, and immune interactions and may influence disease progression. This study aimed to assess circulating adipokines and related microenvironmental mediators as potential biomarkers of disease activity and treatment response in MM. Materials and Methods: In this case-control, cross-sectional study, the serum levels of eight adipokine-related molecules-adiponectin, leptin, resistin, chemerin, adipsin, thrombospondin-1 (TSP-1), paraoxonase-1 (PON-1), and myeloperoxidase (MPO)-were measured in 40 MM patients and 38 age- and sex-matched healthy controls. Enzyme-linked immunosorbent assays (ELISA) and bead-based multiplex immunoassays were used. Associations with prognostic markers (serum β2-microglobulin (sB2M), LDH, albumin, hemoglobin, renal function) and treatment response were analyzed using correlation and non-parametric statistical methods. Results: Compared to the controls, MM patients exhibited significantly higher circulating levels of adiponectin, resistin, chemerin, adipsin, TSP-1, and MPO, while leptin was decreased. Among clinical correlations, chemerin and PON-1 correlated positively with sB2M, TSP-1 correlated with LDH, and MPO correlated with M-protein and albumin. Resistin was lower in patients with renal impairment and an advanced disease stage. Adiponectin and TSP-1 were significantly lower in progressive disease compared to complete remission, suggesting their potential association with treatment response. Conclusions: This study demonstrates that multiple adipokines are dysregulated in MM and exhibit distinct associations with disease burden, renal function, and therapeutic response. Novel associations identified for TSP-1, PON-1, and adipsin highlight previously unrecognized microenvironmental pathways in MM biology. Adipokine profiling may complement established prognostic markers and provide new insights into the tumour microenvironment in MM.

General Background: Autoimmune thyroid diseases (ATDs), such as Graves’ disease and chronic autoimmune thyroiditis, are among the most prevalent endocrine disorders characterized by immune-mediated thyroid dysfunction. Specific Background: Cytokines and immune markers play pivotal roles in the pathogenesis of ATDs, yet their association with hematological indices and ovarian reserve markers, such as Anti-Müllerian Hormone (AMH), remains underexplored. Knowledge Gap: Despite the known role of interleukins in autoimmune conditions, limited data exist linking IL-10, IL-17, and IL-18 levels with hematological and reproductive parameters in ATD patients. Aims: This study aimed to assess immunological (IL-10, IL-17, IL-18, AMH) and hematological (Hb, WBC, PLT) parameters in ATD patients compared to healthy individuals. Results: Findings revealed significantly higher serum IL-10, IL-17, and IL-18 levels in ATD patients, while AMH and hemoglobin were markedly reduced. White blood cell and platelet counts were significantly elevated, suggesting immune-driven hematopoietic alterations. Novelty: This study provides integrated evidence linking cytokine dysregulation with hematological and ovarian reserve disturbances in ATD, highlighting potential biomarkers for disease activity. Implications: The results underscore the need for cytokine profiling in ATD management and suggest that IL-10 and IL-18 may serve as predictive indicators for immune and reproductive dysfunction in affected individuals.Highlight : The study found significant increases in IL-10, IL-17, and IL-18 levels among patients with autoimmune thyroid disorders. Patients showed lower AMH and hemoglobin levels, with higher WBC and platelet counts compared to controls. These results emphasize the role of cytokines in immune and hematological alterations associated with autoimmune thyroid disease. Keywords : Autoimmune Thyroid Dysfunction, IL-18, IL-17, AMH, IL-10

Crohn’s disease (CD) and ulcerative colitis (UC) are two types of inflammatory bowel diseases (IBD) diagnosed by chronic inflammation of the gastrointestinal system. Despite being the gold standard for assessing the therapeutic response to biological medicines like infliximab and disease activity in IBD patients, endoscopy's widespread use is limited by its time-consuming, expensive, and intrusive nature. This prospective case-control study was performed at Ain Shams University School of Medicine Hospital to examine the clinical utility of serum oncostatin M (OSM) as a biomarker for disease activity and response to infliximab in Egyptian IBD patients. It included 72 IBD patients (19 CD, 53 UC) and 29 controls. Patients were divided into three groups to investigate the connection between disease activity and OSM levels. To analyze the connection between OSM expression and clinical response, 36 IBD patients (22 with UC and 14 with CD) receiving infliximab maintenance were enrolled. All patients were subjected to comprehensive medical history, clinical evaluation, endoscopies, and detection of serum OSM levels. Of the 36 IBD patients, 18 patients responded to infliximab treatment, while the other 18 patients did not. The results demonstrated that, in comparison to controls, patients with IBD had higher levels of serum OSM expression. Serum OSM levels in IBD patients showed a positive association with disease activity. Individuals with moderate-to-severe UC and active CD had considerably elevated levels compared to those in remission. In conclusion, serum OSM showed as a promising biomarker for managing individuals with IBD, it was substantially expressed and positively connected with the severity of the disease. Infliximab non-response was linked to elevated OSM levels.

Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system characterized by inflammation and demyelination. Cytokines play a key role in MS pathogenesis and may serve as potential biomarkers for disease activity. The objective of this study was to compare the serum concentrations of IL-2, IL-4, IL-1RA, IL-1β, TNFα, and IFNγ in Saudi MS patients with matched healthy controls using LUMINEX assay. Moreover, it investigated these levels more closely between the MS and patient groups to evaluate the inter-relationships between them and investigate their possible relevance in the pathogenesis of the disease. All subjects (controls and patients) had their serum samples taken. The MILLIPLEX® Human Cytokine/Chemokine/Growth Factor Panel was used in a 96-well plate assay. The Z-test and Pearson's correlation coefficient were employed in SPSS Version 26.0 for Windows to determine the differences in serum cytokine concentrations between the two groups and the correlation between serum and inflammatory mediators in MS patients with a significance threshold of p < 0.05. Most patients (73.7 %) were female, while 26.3 % were male. In the healthy control group, 81.8 % were women and 18.2 % were men. Female MS patients had an average age of 29.6 ± 7.7 years, whereas male patients averaged 33.9 ± 5.6 years. In healthy controls, females had an average age of 35±11.5 years, and males had an average age of 24±0.1 years.MS patients showed no statistical significance regarding the tested inflammatory cytokines IL-1RA, IL-4, IL-2, IFNg, TNFa, and IL-1β (p > 0.05). IL-1β level was moderately positively correlated with IL-2 (r = 0.546, p = 0.000). IL-1RA levels showed a strong positive correlation with IL-2 (r = 0.756, p = 0.000) and were moderately negatively correlated with IL-4 (r =-0.444, p = 0.001). IL-1RA levels exhibited a moderate negative correlation with IL-4 (r=-0.362, p = 0.005) and a strong positive relationship with IFNg (r = 0.809, p = 0.000) and TNFa (r = 0.805, p = 0.000). The study findings showed elevated IL-1RA and IL-2 biomarkers in MS patients without any statistical significance. We observed positive correlations among IL-1RA, IL-2, IFNg, and TNFa and a negative correlation with IL-4, suggesting a Th1-dominant response.

Crohn's disease (CD) and ulcerative colitis (UC) are two types of inflammatory bowel diseases (IBD) diagnosed by chronic inflammation of the gastrointestinal system. Despite being the gold standard for assessing the therapeutic response to biological medicines like infliximab and disease activity in IBD patients, endoscopy's widespread use is limited by its time-consuming, expensive, and intrusive nature. This prospective case-control study was performed at Ain Shams University School of Medicine Hospital to examine the clinical utility of serum oncostatin M (OSM) as a biomarker for disease activity and response to infliximab in Egyptian IBD patients. It included 72 IBD patients (19 CD, 53 UC) and 29 controls. Patients were divided into three groups to investigate the connection between disease activity and OSM levels. To analyze the connection between OSM expression and clinical response, 36 IBD patients (22 with UC and 14 with CD) receiving infliximab maintenance were enrolled. All patients were subjected to comprehensive medical history, clinical evaluation, endoscopies, and detection of serum OSM levels. Of the 36 IBD patients, 18 patients responded to infliximab treatment, while the other 18 patients did not. The results demonstrated that, in comparison to controls, patients with IBD had higher levels of serum OSM expression. Serum OSM levels in IBD patients showed a positive association with disease activity. Individuals with moderate-to-severe UC and active CD had considerably elevated levels compared to those in remission. In conclusion, serum OSM showed as a promising biomarker for managing individuals with IBD, it was substantially expressed and positively connected with the severity of the disease. Infliximab non-response was linked to elevated OSM levels.

Introduction. Lupus erythematosus (LE) is a heterogeneous autoimmune disease, and pro-inflammatory cytokines play important roles in its pathogenesis. Despite numerous studies, the features of the cytokine profile in cutaneous LE (CLE), as well as its changes in response to plasmapheresis, remain unclear.Aim. To assess the levels of IL-17A, IL-31, IL-13 and IL-10 in patients with discoid (DLE) and systemic (SLE) LE, as well as changes in their levels at different time points after membrane plasmapheresis.Materials and methods. The study included 30 patients (21 with DLE, 9 with SLE), who were treated at the Moscow Scientific and Practical Center for Dermatovenereology and Cardiology of the Moscow Health Department. Cytokine levels were assessed before treatment, after the first plasmapheresis procedure, and at 14 days. The results were compared with reference values.Results. Patients with DLE showed elevated levels of IL-17A and IL-31 at baseline. After the first procedure, a decrease in IL-17A and IL-13 with a sharp increase in IL-31 were observed. At 14 days, IL-17A and IL-10 levels continued to decrease, IL-13 levels recovered to baseline, and IL-31 levels remained elevated. In patients with SLE, a moderate decrease in IL-17A and an increase in IL-13 and IL-10 were observed. At 14 days, IL-17A and IL-10 levels decreased, IL-13 levels demonstrated significant fluctuations, and IL-31 levels remained stable in both cases.Conclusions. Plasmapheresis has been shown to have a modulating effect on cytokine levels in patients with LE. IL-31 and IL-10 can be considered potential biomarkers of disease activity and systemic progression. The data obtained support the feasibility of plasmapheresis in the therapy of resistant forms of LE.