Signal transducer and activator of transcription 1 (STAT1) mutations are associated with diverse pathologies. Loss-of-function (LOF) heterozygous mutations impair interferon (IFN) signaling, predisposing to Mendelian susceptibility to mycobacterial diseases (MSMDs). This study characterizes a novel STAT1 LOF mutation in a patient with multisystem manifestations. A patient presenting with mycobacterial infection, skeletal abnormalities, and systemic inflammation underwent whole-exome sequencing. The identified STAT1 variant was analyzed via computational tools (PolyPhen-2/SIFT). Molecular biological validation included IFN-α/γ-induced STAT1 phosphorylation assays and fluorescence microscopy for subcellular localization. Clinical features included mycobacterial osteomyelitis, severe rash, dwarfism, hepatosplenomegaly, and elevated inflammatory markers (C-reactive protein/erythrocyte sedimentation rate). A heterozygous STAT1 mutation (NM_007315.4:c.2120T>C; p.Ile707Thr) was identified and predicted as pathogenic. Mutant cells showed reduced STAT1 phosphorylation (64% versus wild-type, < 0.05) and impaired nuclear translocation post-IFN-α/γ stimulation. Antibiotic therapy achieved clinical resolution without complications. These findings indicated that the STAT1 I707T mutation disrupts IFN-α/γ immunity, expanding the MSMD genotypic spectrum. Genetic screening for STAT1 defects is critical in patients with mycobacterial infections involving skin. Molecular biological studies corroborate mutation pathogenicity, guiding therapeutic decisions.

Psoriasis is an immune-mediated chronic inflammatory disease characterized by keratinocyte hyperproliferation and inflammatory cell infiltration. While noncoding RNAs are implicated in its progression, research remains limited. Integrating lncRNA microarray data with LncRNASNP2-based predictions identified the long noncoding RNA (lncRNA) as a potential functional lncRNA contributing to psoriasis pathogenesis. This study aimed to investigate the role of lnc-/miR-145-5p/fibronectin (FN1) axis in psoriasis. We found that was significantly upregulated in psoriatic tissues. In a psoriasis cell model established by stimulating NHEKs and HaCaT cells with the M5 cytokine cocktail (IL-17A, IL-22, oncostatin M, IL-1α, and TNF-α), lnc-HSFY2-10:1 promoted keratinocyte hyperproliferation and CCL20 secretion. Mechanistically, functioned as a competitive endogenous RNA for miR-145-5p, thereby regulating FN1 expression. Overexpression of miR-145-5p markedly reversed the -induced upregulation of FN1, keratinocyte proliferation, and CCL20 secretion. These findings indicate that the lnc-/miR-145-5p/FN1 axis plays a crucial role in psoriasis pathogenesis and serves as a potential therapeutic target. [Figure: see text].

Myocardial infarction (MI) triggers a systemic inflammatory response that influences cardiac recovery. Pharmacological therapies, including aspirin, β-blockers, Angiotensin-Converting Enzyme (ACE) inhibitors, statins, and P2Y12 inhibitors such as Ticagrelor, may have additional immunomodulatory effects beyond their primary cardiovascular benefits. This study evaluates the impact of different treatment regimens on inflammatory markers, immune cell phenotyping, and cardiac biomarkers in MI patients. A total of 78 MI patients were divided into three treatment groups: standard therapy (aspirin + β-blockers), enhanced therapy (aspirin, β-blockers, ACE inhibitors, and statins), and experimental therapy (Ticagrelor + standard therapy). Inflammatory cytokines (Interleukin (IL)-4, IL-6, IL-10, IL-17, Interferon (IFN)-γ, Tumor Necrosis Factor (TNF)-α, Transforming Growth Factor (TGF)-β), cardiac biomarkers [Troponin, B-type natriuretic peptide (BNP)], and immune cell profiles (Th1/Th2 balance) were assessed using Enzyme-Linked Immunosorbent Assay (ELISA), qPCR (Polymerase Chain Reaction), and flow cytometry before and after treatment. Pro-inflammatory markers (IL-6, TNF-α, IFN-γ, IL-17) significantly decreased, while anti-inflammatory cytokines (IL-4, IL-10, TGF-β) increased post-treatment ( < 0.0001). Th1 cell proportions declined, with a concurrent rise in Th2 cells, particularly in enhanced and experimental therapy groups. Troponin and BNP levels decreased, indicating reduced myocardial stress. Pharmacological therapies effectively modulate immune responses, suppress inflammation, and promote myocardial recovery. Ticagrelor demonstrated additional anti-inflammatory benefits, suggesting potential for improved post-MI outcomes. Future studies should explore long-term clinical implications of immune-targeted cardiovascular therapy.

Bushen Huoxue Acupuncture shows potential in treating neurodegenerative diseases, but its mechanisms remain incompletely understood. Using the senescence-accelerated mouse-prone 8 (SAMP8) mouse model, we assessed cognitive function via the Morris water maze test, hippocampal neuronal apoptosis with terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and microglial activation through immunohistochemistry. Serum levels of inflammatory cytokines [tumor necrosis factor-alpha, interleukin (IL)-1β, and IL-6] were quantified by enzyme-linked immunosorbent assay. The expression of SIRT2 pathway-related proteins, along with Aβ deposition, was analyzed using Western blotting, immunohistochemistry, and immunofluorescence. The results demonstrated that Bushen Huoxue Acupuncture improved cognitive function in SAMP8 mice, reducing hippocampal neuronal apoptosis and decreasing serum levels of pro-inflammatory cytokines. Additionally, it reduced the levels of Aβ42, a more aggregation-prone and toxic Aβ subtype, in both hippocampal tissues and serum, as well as the number of CD68-positive cells in hippocampal tissues, suggesting the inhibition of amyloid pathology and neuroinflammatory. The treatment also downregulated SIRT2, BACE1, and APP-CTF while increasing RTN4B expression. Notably, Bushen Huoxue Acupuncture outperformed non-acupoint acupuncture in enhancing cognitive function and reducing inflammation. Our findings indicate that Bushen Huoxue Acupuncture alleviates cognitive deficits and neuroinflammation by suppressing the SIRT2-mediated RTN4B/BACE1 pathway, highlighting acupuncture as a promising therapy for neurodegenerative diseases.

This study aims to screen liquid-liquid phase separation (LLPS)-related genes modulating ubiquitination for diagnosing patients with diabetic nephropathy (DN). After performing differential gene expression analysis, ssGSEA, and immune infiltration analysis, LLPS-related genes modulating ubiquitination, key immune cells, and immune-related pathways were acquired. The correlations between LLPS-related genes and ubiquitination, key immune-related pathways were explored, respectively. The diagnostic genes were identified by four machine learning algorithms, followed by evaluation to predict the performance of the machine learning models on ubiquitination using receiver operating characteristic curves and a confusion matrix. experiments were applied to explore the function of signal transducer and activator of transcription 1 () in DN. Totally, 513 differentially expressed genes were screened between the DN and control groups. The activity of the ubiquitin-mediated proteolysis pathway exhibited a significant difference between the DN and control samples. The fraction of a total of 10 immune cells exhibited a significant difference between the lower and higher ubiquitination groups. Totally, nine LLPS-related genes modulating ubiquitination were acquired, and these genes modulating ubiquitination were enriched in ubiquitin pathways and significantly positively correlated with the complement, IFN-α, and IFN-γ pathways. Two diagnostic genes were obtained, namely dual specificity tyrosine phosphorylation regulated kinase 2 () and . Notably, downregulation of effectively alleviated , , , and levels in D-glucose-treated HK-2 cells, as well as the protein level of FK2. LLPS-related modulating ubiquitination accelerates the inflammatory response in DN.

This study was conducted to investigate the protective effect of platelet-rich plasma-derived exosomes (PRP-Exos) in diabetic wound healing, as well as the involved molecular mechanism. Exosomes collected from PRP were extracted and identified, then the promoting effect on diabetic wound healing was tested in high glucose and lipopolysaccharide (HL)-induced RAW264.7 cells and excisional wound models constructed in streptozotocin-induced diabetic SD rats. PRP-Exos showed the best capacity for accelerating wound healing in the diabetic rat model. Cell proliferation of RAW264.7 cells was effectively facilitated after HL treatment, while PRP-Exos implemented could obviously eliminate the HL effect on RAW264.7 cells. The protein expression levels of PINK1, parkin, and LC3I/LC3II were both obviously diminished, and the expression of kininogen-1 (KNG1) was obviously increased in HL-induced RAW264.7 cells, while the opposite results were observed after PRP-Exos treatment. HL treatment could remarkably suppress the protein expression levels of p-PI3K/PI3K and p-AKT/AKT in RAW264.7 cells, while PRP-Exos administration could reverse this trend. Interestingly, KNG1 upregulation could effectively reverse the effect of PRP-Exos on the tumor necrosis factor-alpha and high mobility histone 1 levels, protein expression of p-PI3K/PI3K and p-AKT/AKT, and mitophagy-related markers in HL-induced RAW264.7 cells. In conclusion, PRP-Exos facilitated macrophage mitophagy in diabetic wound healing by targeting KNG1 via PI3K-AKT pathway.

Hirudin, a polypeptide extracted from medicinal leeches, has demonstrated potential in treating renal fibrosis. This study aimed to explore the underlying mechanisms by which Hirudin alleviates renal fibrosis. Renal fibrosis models were established using unilateral ureteral obstruction (UUO) surgery in rats and transforming growth factor-β (TGF-β)-induced HK-2 cells, followed by treatment with different concentrations of Hirudin. Renal function indicators were detected using an automatic analyzer. Renal pathology was observed using hematoxylin-eosin and Masson staining, and α-smooth muscle actin (α-SMA) (a fibrosis marker) expression was detected by immunohistochemistry. Cell viability was tested using cell counting kit-8 assay. Western blot was utilized to detect α-SMA, NOD-like receptor thermal protein domain associated protein 3 (NLRP3), Gasdermin D (GSDMD), cleaved caspase-1, phosphorylated mammalian target of rapamycin (p-mTOR), mammalian target of rapamycin (mTOR), and hypoxia-inducible factor-1α (HIF-1α) levels. Interleukin (IL)-1β and IL-18 levels were measured using enzyme-linked immunosorbent assay (ELISA). UUO rats exhibited impaired renal function and severe renal fibrosis, accompanied by increased NLRP3, GSDMD, cleaved caspase-1, IL-1β, IL-18, p-mTOR/mTOR, and HIF-1α levels. Hirudin alleviated renal fibrosis, reduced pyroptosis, and inhibited mTOR/HIF-1α pathway in UUO rats. TGF-β stimulation decreased cell viability, increased α-SMA expression and pyroptosis, and activated mTOR/HIF-1α pathway in HK-2 cells. These changes were reversed by Hirudin. However, the mTOR agonist MHY1485 altered the effects of Hirudin. In conclusion, Hirudin reduces pyroptosis to alleviate renal fibrosis, potentially by suppressing mTOR/HIF-1α pathway.

C-X-C chemokine receptor 4 (CXCR4) is a chemokine receptor. Paired box protein 5 (PAX5) is a nuclear transcription factor. Octamer-binding protein 2 (OCT2) is a B-cell-restricted transcription factor. This study aimed to evaluate the protein expression of CXCR4, PAX5, and OCT2, as well as the gene expression of long noncoding RNA (lncRNA) X-inactive specific transcript (XIST)/miR-34/PAX5, in diffuse large B-cell lymphoma (DLBCL). The study included 67 patients with DLBCL and 15 lymphoid tissue samples from reactive lymph nodes. Immunohistochemical (IHC) methods were used to evaluate protein expression. Gene expression was measured by real-time polymerase chain reaction. Correlation analysis showed significant negative correlations between miR-34 expression and each of the expression (r = -0.41, < 0.001) and expression (r = -0.43, < 0.001). At the same time, there was a strong positive correlation between expression and expression (r = 0.92, < 0.001). In conclusion, our findings indicate that CXCR4, OCT2, and PAX5 IHC expressions can be considered diagnostic markers in DLBCL. In addition, the axis may serve as a potential diagnostic marker in DLBCL. Moreover, CXCR4 and expressions may be potential prognostic markers in DLBCL.

Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related deaths worldwide. The genomic database for NSCLC is expanding rapidly, highlighting the importance of characterizing subpopulations from diverse regions. This study aims to identify and correlate genomic variants in patients with non-squamous NSCLC from two cities in Paraná, Brazil, and compare these findings with data from The Cancer Genome Atlas (TCGA) and the broader Brazilian population. We conducted a retrospective study sequencing tumor sample from 133 patients. An analysis was performed for gene functional analysis. Additional data on tumor mutational burden (TMB), microsatellite status, and clinicopathological characteristics were also collected. The mutational load in the studied population was comparable to that of the TCGA cohort. However, gene expression profiles differed significantly, particularly for the EGFR, TP53, KRAS-NRAS, STK11-KEAP1, MTAP-CDKN2A/B, and PDL-1 genes. The gene expression profile in this study also showed marked differences from the general Brazilian population, with notably higher expression rates of EGFR and PDL-1. Specifically, considering the PDL-1 expression levels, 14% were classified as hyper-expressors, 33% as hypo-expressors, and 52% as non-expressors. These proportions were statistically distinct from global literature but aligned with the Brazilian profile. The genomic profile of patients with NSCLC in Paraná reveals a regional signature, characterized by a higher frequency of EGFR and TP53 mutations, along with elevated PDL-1 expression. These findings highlight the potential for regional variations in NSCLC, which could inform personalized treatment strategies for this population.

We aimed to measure serum concentrations of interleukin (IL) 8, tumor necrosis factor-α (TNF-α), IL-6, IL-1β, and human neutrophil gelatinase-associated lipocalin (N-gal) in children with Shiga toxin-producing (STEC) infection to determine the inflammatory cytokine profile and the role of these molecules in hemolytic uremic syndrome (HUS) development and severity. Three groups of patients with evidence of STEC infection were incorporated: bloody diarrhea (BD), patients with HUS requiring dialysis (HUSD), and patients with HUS and no dialysis requirement (HUSND). Serum samples were assayed for cytokines and N-gal using immunoassays. Thirty-six children were enrolled: 13 with BD, 10 with HUSND, and 13 with HUSD. We found significantly higher levels of IL-8, TNF-α, IL-6, and N-gal in patients with HUSD compared to patients with BD. Only TNF-α levels were significantly higher in patients with HUSND than in patients with BD. Higher IL-8 and N-gal levels were evidenced in HUSD than in patients with HUSND at the initial stages of disease. Principal component analysis revealed that children with HUSD exhibited an immune profile different from the other study groups. These results suggest a possible involvement of IL-8 in disease severity in patients with STEC-HUS. Furthermore, our results indicate a potential role of N-gal in HUS development. [Figure: see text].

The pro-apoptotic and pro-inflammatory effects of FK506 binding protein 5 (FKBP5) in sepsis-induced acute kidney injury have been previously reported. However, its biological functions and underlying mechanisms in regulating sepsis-induced intestinal injury remain elusive. Therefore, this study aimed to explore the effects of FKBP5 on sepsis-induced intestinal injury. A mouse model of sepsis was established by cecal ligation and puncture (CLP). A cell model was established by treating Caco-2 cells with lipopolysaccharide (LPS). The impacts of FKBP5 knockdown on apoptosis, barrier integrity, inflammation, and the nuclear factor kappa B (NF-κB) signaling were evaluated in ileal tissue and Caco-2 cells. FKBP5 expression was elevated in the ileal tissue in response to CLP and LPS treatments. In mice with sepsis, FKBP5 knockdown reduced cell apoptosis and regulated Bax, Bcl-2, and cleaved PARP levels. FKBP5 knockdown also reduced the levels of D-lactic acid, tumor necrosis factor alpha, interleukin (IL)-6, and IL-1β, improved intestinal histopathological damage, and enhanced the expression of zonula occludens-1 and occludin. FKBP5 knockdown also displayed protective effects in LPS-stimulated cells. FKBP5 knockdown inhibited the NF-κB signaling in CLP and LPS groups. Inhibition of FKBP5 alleviates inflammation and intestinal barrier dysfunction in sepsis, partially by inhibiting the NF-κB signaling.

This prospective study investigated the utility of baseline CXCL13 levels in predicting methotrexate response and monitoring disease activity in 50 treatment-naive early rheumatoid arthritis (RA) patients (2010 American College of Rheumatology/European League Against Rheumatism criteria) treated with methotrexate. Participants were categorized into methotrexate responders (MTX-R, = 29) and nonresponders (MTX-NR, = 21) at 12 weeks. Baseline CXCL13 levels were significantly higher in MTX-R compared with MTX-NR ( = 0.035). Receiver operating characteristic curve analysis identified a baseline CXCL13 cutoff of >100 pg/mL for predicting methotrexate response, with 69% sensitivity, 52% specificity, and 62% accuracy. Posttreatment, CXCL13 levels decreased significantly in MTX-R ( < 0.001) but remained unchanged in MTX-NR. Disease activity parameters (eg, DAS-28) correlated with CXCL13 dynamics, though specific coefficients were not detailed. The study highlights CXCL13 as a potential biomarker for stratifying methotrexate therapy, with higher baseline levels favoring therapeutic response and posttreatment reductions reflecting clinical improvement. While moderate diagnostic accuracy limits standalone use, CXCL13 may complement existing tools to guide early personalized treatment. Further validation in larger cohorts is warranted to confirm its role in optimizing RA management.

Listeriosis is a foodborne disease caused by (Lm) that usually leads to serious adverse outcomes in pregnant women. Interleukin (IL)-33/serum stimulation (ST)2 axis has an important impact on infectious diseases, but its role in listeriosis is rarely studied. Here, the immunomodulatory effects of IL-33/ST2 axis during perinatal Lm infection were investigated. In our study, the perinatal Lm infection model was constructed by injecting Lm into the tail vein of C57BL/6J mice. IL-33/ST2 axis was blocked by intraperitoneal injection of anti-IL-33Rα/ST2 antibody. , mouse cytotoxic T lymphocyte cell line (CTLL)-2 cells were activated by using CD3/CD28 antibodies. Perinatal Lm infection caused massive necrosis of liver tissue. Blocking IL-33/ST2 axis in pregnant mice inhibited the infiltration of CD8 T lymphocytes into the site of infection and further aggravated liver damage. We also found that IL-33 promotes mitochondrial autophagy in activated CTLL-2 cells . Mitochondrial autophagy was beneficial to the clearance of damaged mitochondria and reduced the production of reactive oxygen species. IL-33/ST2 axis affects the immune function of CD8 T lymphocytes by regulating mitophagy, which plays a very important role in the occurrence and development of perinatal Lm infection. Immunomodulation targeting IL-33/ST2 axis may be an effective way to adjuvant treatment of perinatal Lm infection.

The presence of circulating cytokines has a significant impact on the development and progression of vestibular disorders. However, further investigation is needed to determine the direction of causation and causal effects. By applying two-sample Mendelian randomization (MR), we analyzed the potential causal connection between 41 circulating cytokines and vestibular disorders using the integrated data from genome-wide association studies (GWAS). The major analysis utilized for MR was inverse variance weighted (IVW). To examine reverse causation, we conducted reverse MR analysis. In addition, we assessed the robustness of the findings by performing pleiotropy and heterogeneity tests. Our results demonstrated that two circulating cytokines were significantly correlated with vestibular disorders risk. More specifically, vascular endothelial growth factor [IVW, odds ratio (OR) = 0.999, 95% confidence interval (CI) = 0.999-1.000, = 0.046] and interleukin-7 (IVW, OR = 0.999, 95% CI = 0.998-1.000, = 0.033) were negatively correlated with vestibular disorders risks, respectively. No evidence was identified to support associations between the remaining 39 circulating cytokines and vestibular disorders. These findings reveal a distinct correlation between circulating cytokines and vestibular diseases, providing a novel perspective and potential biological target for future clinical interventions for vestibular disorders.

The expansion of social media has fundamentally transformed biomedical research dissemination and collaboration, particularly within the interferon and cytokine research community. This paper explores recent trends (2024-2025) that have amplified the role of platforms such as Twitter (now "X"), LinkedIn, Mastodon, Threads, and Bluesky. These tools have facilitated rapid knowledge exchange, democratized access to scientific discourse, enabled diverse voices to participate meaningfully, and fostered cross-disciplinary and global collaborations. Additionally, the integration of preprint repositories like bioRxiv and medRxiv, along with the evolution of open access publishing, further accelerates the accessibility and immediacy of scientific communication. Despite evident benefits, the rapid dissemination facilitated by social media also poses ethical challenges, including concerns about misinformation, premature dissemination of preliminary data, and privacy considerations. Practical strategies for researchers and institutions to effectively navigate these platforms responsibly are presented, aiming to optimize the impact of social media on scientific discovery and public engagement.

Kawasaki disease (KD) is an acute childhood vasculitis, commonly seen in children under the age of five. Despite extensive research over the past five decades, the pathogenesis of KD remains elusive. The objective of this epigenetic reanalysis study is to delineate common pathways involved in KD using a bioinformatics approach. Array datasets from the Gene Expression Omnibus repository were extracted and subjected to analysis using the Chip Analysis Methylation Pipeline in the R statistical tool for the identification of differential methylation probes and differential methylation regions. Adaptive immune genes , and were significantly hypermethylated in acute KD as compared to healthy controls. Gene enrichment analysis showed that genes involved in T-cell receptor activation and differentiation, antigen processing and presentation of MHC class I were hypermethylated, whereas neutrophil degranulation was hypomethylated in the acute phase of KD as compared to healthy controls. The proportion of neutrophils significantly increased, while the proportions of CD4 T-cells and CD8 T-cells decreased in the peripheral blood of children with acute KD as compared to healthy controls. Reduced proportions of CD4 T cells and CD8 T cells, as well as hypermethylation of their genes, have been observed in the peripheral blood of patients with acute KD.

The association between local oral inflammation and cardiovascular risk has been extensively studied, with results indicating a bidirectional relationship. The aim of the present study was to investigate the associations between blood cells and a large number of salivary cytokines, chemokines, and growth factors. The study consisted of 165 individuals who were referred to the Oral and Maxillofacial Surgery clinic at Falun County hospital, Sweden, for surgical removal of impacted lower third molar. The study subjects did not have any known inflammatory disorders. Complete blood cell counts were analyzed using the routine laboratory at Falun Hospital, Falun, Sweden. Proteomic analysis of 92 inflammation-related protein biomarkers in saliva was performed using a multiplex proximity extension assay. After adjustment for multiplicity testing using the false discovery rate approach, there remained significant association between several saliva cytokines, chemokines, and growth factors and white blood cell counts ( = 19), neutrophil counts ( = 18), erythrocyte counts ( = 13), hemoglobin concentrations ( = 20), erythrocyte volume fractions ( = 22), and platelet counts ( = 12). There are several significant associations between local inflammatory cytokines in the oral cavity and blood cell parameters indicating a relationship between local and systemic inflammatory activity.

Lumbar disc herniation is primarily caused by intervertebral disc degeneration (IVDD). Nucleus pulposus (NP) cell dysfunction leads to pro-inflammatory cytokines secretion increase, causing extracellular matrix (ECM) degradation. ECM is essential for maintaining normal disc function. Glycoprotein (Transmembrane) Nmb (GPNMB) is strongly associated with inflammation, and its expression and effects in IVDD are unclear. We categorized 40 clinically collected IVDD samples using the magnetic resonance imaging (MRI)-based Pfirrmann grading system. GPNMB mRNA expression was notably suppressed in patients with severe IVDD compared with patients with mild IVDD. Increased GPNMB mRNA expression correlated with decreased Interleukin-6 (IL-6) expression and increased collagen type II (COL2A1) expression levels. We utilized lentivirus to overexpress GPNMB in IL-1β-induced NP cells to explore its function in IVDD. GPNMB overexpression inhibited pro-inflammatory cytokines Tumor necrosis factor-alpha and IL-6 secretion in IL-1β-induced NP cells, while anti-inflammatory cytokine IL-10 content was increased. In addition, GPNMB overexpression inhibited NP ECM degradation by decreasing ECM-degrading enzymes matrix metalloproteinases-3/13 and a disintegrin and metalloproteinase with thrombospondin motifs-4/5 . Mechanism studies revealed that GPNMB was bound to CD44, a receptor expressed on the NP cell surface. GPNMB overexpression inhibited nuclear factor-κB (NF-κB) p65 phosphorylation and nuclear translocation , possibly through CD44. In conclusion, GPNMB suppressed the expression of pro-inflammatory cytokines and ECM degradation in NP cells by inhibiting activation of NF-κB.

Dysregulation of immune cells and cytokines, particularly T helper 17 (Th17) cells and their associated cytokines, is implicated in the pathogenesis of both systemic lupus erythematosus (SLE) and chronic kidney disease (CKD). This study aimed to investigate the serum levels of Th17-related cytokines (interleukin [IL]-17A, IL-21, IL-22, and IL-23) in CKD patients with and without SLE and explore their potential role in disease progression. A total of 118 participants were included, comprising 78 patients with CKD (stages 3-5) and 40 healthy controls. Cytokine levels were measured using enzyme-linked immunosorbent assay kits. Patients with CKD exhibited significantly lower IL-21 levels and higher IL-22 and IL-17A levels compared with controls, while patients with end-stage renal disease showed elevated IL-21 and IL-23 levels. Among SLE-negative nephrotic patients, IL-23 and IL-17A were significantly upregulated, whereas SLE-positive nephrotic patients had increased IL-22 and IL-17A levels. In addition, IL-21 and IL-17A were significantly correlated in patients with CKD, suggesting a potential immunoregulatory interplay. These findings indicate that Th17-related cytokines are differentially expressed depending on CKD stage and SLE status, potentially influencing immune responses, inflammation, and kidney fibrosis. Understanding alterations of these cytokines may aid in identifying targeted therapeutic, particularly for patients with CKD at risk of SLE-related complications.