Objective To investigate the prevalence and clinical significance of the centromere protein-F-like(CENP-F-like)immunofluorescence staining pattern in a large patient cohort and through literature review.Methods We retrospectively analyzed antinuclear antibody(ANA)immunofluorescence assay results from 191 274 patients at West China Hospital of Sichuan University between March 2018 and November 2020.Specific immunological markers were tested in sera with CENP-F-like patterns.Additionally,a narrative review of seven relevant studies was performed for comparison.Results In Southwest China,ANA positivity was found in 32.09%of patients,with the CENP-F-like pattern detected in 0.015%of all cases and 0.05%of ANA-positive individuals.The CENP-F-like pattern appeared predominantly at titers≥1∶320,most often in isolation(68.97%),but also mixed with cytoplasmic speckled patterns.Patients with cancers accounted for the highest proportion(31.03%),including solid tumors and hematologic malignancies.Metastasis was observed in patients with solid tumors,while graft-versus-host disease(GVHD)occurred in those with hematologic malignancies post-transplantation.Autoimmune diseases(AIDs)were diagnosed in 20.69%of cases,all showing disease-specific autoantibodies.These findings were broadly consistent with previous reports and suggest a possible association between the CENP-F-like pattern and malignancies.Conclusion The CENP-F-like pattern is rare in ANA tests but may be associated with clinically important conditions,particularly cancers and AIDs.The occurrence of metastasis and GVHD in patients with this pattern highlights its potential clinical relevance,and concurrent autoantibodies may assist in diagnosing AIDs.

BACKGROUND:Neurosyphilis can trigger neuro-specific immune responses, but evidence remains scarce. This study investigates the prevalence and clinical significance of neural antibodies in neurosyphilis, with a focus on CV2/CRMP5 antibodies. METHODS:We retrospectively analyzed 1149 patients with syphilitic neurological symptoms. Of 247 diagnosed with neurosyphilis, 215 met inclusion criteria. Using CBA and line blot, 97 patients suspected of autoimmune encephalitis were tested for neural antibodies, with positives confirmed by in-house CBA. Complete medical records were collected. Homology between CV2/CRMP5 and Treponema pallidum was assessed via BLAST and structural modeling. RESULTS:Twenty neurosyphilis patients were positive for neural antibodies. Antibodies against neuronal intracellular antigens (NIA-abs) predominated (15/20, 75%), with CV2/CRMP5 being the most frequent (73.3% of NIA-abs). Critically, all CV2/CRMP5-positive cases (11/11, 100%) had parenchymal neurosyphilis (p-NS), and none were found in 86 asymptomatic neurosyphilis (a-NS) patients. In the prospective validation cohort of 115 p-NS patients, 8 CV2/CRMP5-positive cases were identified. Combining retrospective and prospective data, the serum positivity rate of CV2/CRMP5 antibodies in p-NS was 9.79%. These patients exhibited significantly higher serum Toluidine Red Unheated Serum Test (TRUST) titers (median 1:64 vs. 1:16, P < 0.001) and elevated cerebrospinal fluid Immunoglobulin G (CSF IgG) indices (median 2.90 vs. 2.06, P = 0.005) compared to CV2/CRMP5-negative p-NS patients. No homology between CV2/CRMP5 and Treponema pallidum proteins was found. CONCLUSION:Our study identifies a strong association between CV2/CRMP5 antibodies and p-NS. Screening for these antibodies is recommended for p-NS patients, especially those with high serum TRUST titers and intrathecal immunoglobulin synthesis, as they may represent a subgroup with distinct immunopathological mechanisms.

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disorder lacking ideal early diagnostic biomarkers. This study aimed to identify and validate novel microRNAs (miRNAs) in peripheral blood mononuclear cells (PBMCs) as diagnostic biomarkers for SLE. This study comprised a screening stage and a validation stage. We performed high-throughput miRNA sequencing in 3 SLE patients and 3 healthy controls, then validated candidate miRNAs in 39 SLE patients and 40 healthy controls using quantitative real-time polymerase chain reaction (qPCR). Diagnostic performance was assessed using receiver operating characteristic (ROC) curves, and correlations with clinical indicators were analysed. Seventy-eight differentially expressed miRNAs were identified in SLE. Among them, miR-365b-5p and miR-3614-5p were significantly upregulated in SLE PBMCs (both P<0.001). ROC analysis showed area under the curve (AUC) values of 0.733 and 0.782 for the individual models and 0.805 for the combination. MiR-365b-5p was positively correlated with IgM, while miR-3614-5p was associated with immune cell counts, liver and kidney function, and metabolic parameters. Bioinformatics suggested involvement in immune regulation and the MAPK signaling pathway. miR-365b-5p and miR-3614-5p are significantly elevated in SLE and have favourable diagnostic value. These two miRNAs may serve as complementary diagnostic biomarkers that could facilitate early detection, differential diagnosis, and the elucidation of immune pathogenesis in SLE.

OBJECTIVE:This study aimed to identify novel circular RNA (circRNA) biomarkers in peripheral blood mononuclear cells (PBMCs) for the diagnosis of ankylosing spondylitis (AS) and to explore their potential pathogenic mechanisms. METHODS:High-throughput circRNA sequencing was performed on PBMCs from 3 AS patients and 3 healthy controls. Differentially expressed circRNAs were validated by RT-qPCR in an independent cohort (64 AS patients and 24 healthy individuals). Diagnostic performance was evaluated via ROC curve analysis. Correlations between circRNA expression and clinical inflammatory markers were assessed. Bioinformatics analysis was employed to predict target miRNAs and enriched signaling pathways. RESULTS:A total of 53 circRNAs were differentially expressed in AS PBMCs. Among these, circ_0024085 and circ_0000339 were significantly upregulated in AS (41.6-fold and 27.0-fold, p < 0.05), and demonstrated good diagnostic performance (AUC = 0.815 for the combination). The expression of Circ_0024085 was inversely correlated with erythrocyte sedimentation rate (ESR, p = 0.005) and monocyte count (p = 0.027). Bioinformatic analysis indicated that the target miRNAs of circ_0024085 were significantly enriched in the IL‑4/IL‑13 signaling pathway, while those of circ_0000339 were enriched in the SEMA4D signaling pathway. CONCLUSION:Our findings identify circ_0024085 and circ_0000339 as potential diagnostic biomarkers for AS. With bioinformatics predictions indicating that Circ_0024085 may exert an anti-inflammatory effect via M2 macrophage polarization, whereas circ_0000339 might contribute to bone damage through SEMA4D signaling.

Rheumatoid arthritis (RA) is a systemic inflammatory condition posing challenges in identifying biomarkers for onset, severity and treatment responses. Here we investigate the plasma proteome in a longitudinal cohort of 278 RA patients, alongside 60 at-risk individuals and 99 healthy controls. We observe distinct proteome signatures in at-risk individuals and RA patients, with protein levels alterations correlating with disease activity, notably at DAS28-CRP thresholds of 3.1, 3.8 and 5.0. The combination of methotrexate (MTX) and leflunomide (LEF) modulates proinflammatory pathways, whereas MTX plus hydroxychloroquine (HCQ) impact energy metabolism. A machine-learning model is trained for predicting responses, and achieves average receiver operating characteristic (ROC) scores of 0.88 (MTX + LEF) and 0.82 (MTX + HCQ) in the testing sets. The efficiency of these models is further validated in independent cohorts using enzyme-linked immunosorbent assay data. Overall, our study unveils distinct plasma proteome signatures across various stages and subtypes of RA, providing valuable biomarkers for predicting disease onset and treatment responses.

LC-MS-based metabolomics is a powerful tool in analyzing disease molecular mechanisms. Because of its high sensitivity and throughput, LC-MS-based metabolomics usually detects thousands of metabolites. How to find disease-related metabolites and investigate metabolic pathways is critical in metabolomics studies. Conventional statistics-guided data mining looks only for mathematical relations between the detected metabolites and the metadata. It is not enough to unveil biological pathways of metabolites involved in disease progression. Compound similarity network (CSN) is a spectral-independent technique to cluster compounds based on their structural similarities and to investigate potential chemical transformations. Herein, we developed a CSN-assisted metabolic data mining strategy to quantitatively find key metabolites in diseases through structural similarities and explore disease-regulating metabolic pathways based on KEGG and RetroRules metabolic reaction templates. The strategy was used in a metabolomics study of ankylosing spondylitis (AS), in comparison with a healthy cohort and rheumatoid arthritis (RA), a rheumatic disease having similar symptoms with early AS. Using CSN-assisted data mining, a palmitic acid pathway was constructed, which may be regulated in AS pathogenesis.

Rheumatoid arthritis (RA) is a systemic inflammatory joint disease characterized by heterogeneous clinical manifestations, which requires deeper exploration in identifying reliable biomarkers for early diagnosis, monitoring, and treatment assessment. The aim is to discover plasma metabolomic markers to predict RA onset, assess disease activity, and forecast treatment efficacy. The study includes 209 established RA patients who are disease-modifying antirheumatic drugs-free for six months prior to enrollment, with 197 of them followed for 3-6 months to assess treatment response. Additionally, 56 individuals at risk are recruited, with 34 completing a 5-7-year follow-up. Analysis reveals that metabolites related to methylation and redox imbalance, such as S-adenosylmethionine, sarcosine, nicotinamide adenine dinucleotide, glutathione, etc., are associated with RA development and severity, and contribute to its heterogeneity across age, sex, and anti-citrullinated protein autoantibody status. Ridge regression models are constructed using metabolite and clinical features for the response to methotrexate (MTX) plus leflunomide, achieving an average receiver operating characteristic (ROC) score of 0.83, and for the MTX plus hydroxychloroquine, achieving an average ROC score of 0.92. In conclusion, our findings reveal RA metabolomic alterations, aiding early diagnosis and treatment response.

Rheumatoid arthritis (RA) is a chronic autoimmune disease with high disability rates, necessitating early diagnosis. This study investigated the potential of circRNAs, specifically CircRNA_0001412 and CircRNA_0001566, as diagnostic biomarkers for RA. High-throughput transcriptome sequencing was performed on peripheral blood mononuclear cells (PBMCs) from RA patients and healthy controls to identify differentially expressed circRNAs. Reverse transcription quantitative PCR (RT-qPCR) was used to validate circRNA expression in an independent cohort of 78 RA patients and 82 healthy controls. Receiver operating characteristic (ROC) curve analysis was performed to assess the diagnostic value of the selected circRNAs. Correlation analyses with clinical markers such as CRP, ESR, CCP, RF, WBC, lymphocyte count, and monocyte count were also conducted. Bioinformatics analyses, including GO and KEGG pathway enrichment, were conducted to explore the functional roles of the identified circRNAs and associated miRNAs. A total of 54 circRNAs were identified as differentially expressed in RA, with 21 circRNAs upregulated and 33 downregulated. Among these, CircRNA_0001412 and CircRNA_0001566 were highly expressed in RA PBMCs and demonstrated good sensitivity and specificity as diagnostic biomarkers (AUC = 0.751 (95

ObjectiveTo evaluate the concordance of four anti-dsDNA antibody detection methods-Crithidia luciliae indirect immunofluorescence test (CLIFT), enzyme-linked immunosorbent assay (ELISA), acridine ester direct chemiluminescence immunoassay (CLIA), and digital liquid chip method (DLCM)-and to assess their diagnostic efficacy in systemic lupus erythematosus (SLE) patients.MethodsA total of 285 serum samples were collected, including 170 SLE patients, 39 with non-SLE autoimmune diseases (AIDs), 28 with non-AIDs, and 48 undiagnosed cases. The concordance and diagnostic performance of anti-dsDNA antibody methods were analyzed.ResultsThe diagnostic performance showed that DLCM exhibited the highest sensitivity (86.87%), while CLIA demonstrated the highest specificity (94.03%). The area under the receiver operating characteristic (ROC) curve (AUC) was ranked as CLIFT < ELISA < CLIA < DLCM (AUC = 0.938). Anti-dsDNA antibodies detected by both CLIFT and DLCM correlated well with the SLE disease activity index (SLEDAI), while CLIFT and CLIA were significantly correlated with lupus nephritis. Utilizing ROC curve-derived cut-off values, the overall concordance of CLIFT and other methods ranged from 80.14% to 82.58% (kappa > 0.6, P < 0.001), and the concordance between quantitative methods ranged from 89.55% to 91.29% (kappa > 0.8, P < 0.001).ConclusionCLIFT, ELISA, CLIA, and DLCM all showed impressive diagnostic efficacy in detecting anti-dsDNA antibodies. CLIFT shows a strong correlation with SLE activity and lupus nephritis. DLCM, a relatively new method, also showed excellent performance and could be integrated into clinical laboratory workflows for anti-dsDNA antibody testing.

BACKGROUND:Transferrin receptor 1 (TFR1), a major iron receptor for immune cells, could impair T cell metabolism and function in systemic lupus erythematosus (SLE), leading us to investigate the effects of TFR1 and possible mechanisms on lupus B cells. METHODS:B cells from lupus mouse models and systemic lupus erythematosus (SLE) patients were evaluated using flow cytometry (FCM) for levels of TFR1, intracellular iron deposition, reactive oxygen species (ROS), lipid peroxidation, and B-cell subsets. Transcript levels of TFR1 were assessed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and upstream regulatory molecules were identified by in vitro gene silencing. RESULTS:An agonist of toll-like receptor 7 (TLR7), R848 treatment significantly increased TFR1 expression in B cells from C57BL/6 (B6) mice but not those from MRL/lpr mice. In in vitro cultures of mouse splenocytes, TLR7 dose-dependently promoted TFR1 expression, and its effect was probably mediated by P53. Anti-TFR1 antibody effectively inhibited intracellular iron deposition in lupus B cells, reduced ROS and lipid peroxidation, and prevented the production of plasmablasts and autoantibodies. Among different B cell subsets, TFR1 was predominantly expressed in double negative (DN) B cells, with a more pronounced effect on DN2 B cells, which could be normalized by ROS inhibitors. Similarly, in human studies, TFR1 was highly expressed in B cells of SLE patients and closely correlated with TLR7 expression and disease activity scores, as well as iron deposition and ROS production. A significant reduction in ROS production was observed after blocking TFR1. CONCLUSIONS:TLR7-regulated TFR1 may drive B-cell autoimmunity by promoting ROS production, thus contributing to SLE pathogenesis.

ABSTRACTPhysical inactivity and sedentary behavior are associated with higher risks of age‐related morbidity and mortality. However, whether they causally contribute to accelerating biological aging has not been fully elucidated. Utilizing the largest available genome‐wide association study (GWAS) summary data, we implemented a comprehensive analytical framework to investigate the associations between genetically predicted moderate‐to‐vigorous leisure‐time physical activity (MVPA), leisure screen time (LST), and four epigenetic age acceleration (EAA) measures: HannumAgeAccel, intrinsic HorvathAgeAccel, PhenoAgeAccel, and GrimAgeAccel. Shared genetic backgrounds across these traits were quantified through genetic correlation analysis. Overall and independent associations were assessed through univariable and multivariable Mendelian randomization (MR). A recently developed tissue‐partitioned MR approach was further adopted to explore potential tissue‐specific pathways that contribute to the observed associations. Among the four EAA measures investigated, consistent results were identified for PhenoAgeAccel and GrimAgeAccel. These two measures were negatively genetically correlated with MVPA (rg = −0.18 to −0.29) and positively genetically correlated with LST (rg = 0.22–0.37). Univariable MR yielded a robust effect of genetically predicted LST on GrimAgeAccel (βIVW = 0.69, p = 1.10 × 10−7), while genetically predicted MVPA (βIVW = −1.02, p = 1.50 × 10−2) and LST (βIVW = 0.37, p = 1.90 × 10−2) showed marginal effects on PhenoAgeAccel. Multivariable MR suggested an independent association between genetically predicted LST and GrimAgeAccel after accounting for MVPA and other important confounders. Tissue‐partitioned MR suggested skeletal muscle tissue associated variants to be predominantly responsible for driving the effect of LST on GrimAgeAccel. Findings support sedentary lifestyles as a modifiable risk factor in accelerating epigenetic aging, emphasizing the need for preventive strategies to reduce sedentary screen time for healthy aging.

Long non-coding RNAs (lncRNAs) are emerging as critical epigenetic regulators within the gene-environment interaction networks and have been implicated in the progression of rheumatoid arthritis (RA). In the present study, we employed high-throughput RNA sequencing to elucidate the differential expression profiles of lncRNAs in peripheral blood mononuclear cells (PBMCs) from a discovery cohort (3 RA patients vs. 3 healthy controls). Following comprehensive sequencing analysis, 8 lncRNAs were identified as potential biomarkers for RA. Through reverse transcription quantitative polymerase chain reaction (RT-qPCR) validation, we confirmed that LINC01881 (p < 0.01) and MIR3142HG (p < 0.01) exhibited expression patterns consistent with our sequencing results. Both showed moderate diagnostic performance (AUC = 0.713 and 0.723, respectively), and their combination improved diagnostic efficacy (AUC = 0.786). LINC01881 expression was negatively correlated with CRP and ESR, while MIR3142HG correlated positively with platelet count. Bioinformatic analysis suggested that LINC01881 may influence the PI3K-Akt pathway through interactions with PTEN-targeting miRNAs, and MIR3142HG may be involved in hematopoietic and platelet-related processes. In summary, MIR3142HG and LINC01881 are potential diagnostic biomarkers for RA. LINC01881 may act as a compensatory regulator of inflammation via PI3K-Akt signaling, while MIR3142HG may influence platelet biology. Further functional studies are warranted to confirm these mechanisms and explore their clinical utility in multi-marker diagnostic panels.

This review critically evaluates the performance of direct matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) for rapid pathogen identification in life-threatening infections. It aims to assess its application directly from positive blood cultures and sterile body fluids, examine the factors influencing identification success rates, and identify the key challenges limiting its broader clinical implementation. A review of the literature was conducted, focusing on studies utilizing commercial kits or optimized laboratory protocols for direct testing from clinical specimens, including positive blood cultures, cerebrospinal fluid, urine, and enrichment cultures from synovial fluid and ascites. Direct MALDI-TOF MS can deliver reliable pathogen identification within 30–60 minutes, significantly shortening diagnostic turnaround time. However, identification success is not uniform; a consistent performance gradient is observed, with Gram-negative bacteria identified more successfully than Gram-positive bacteria and fungi. This variability reflects differences in microbial cell structure and protein extraction efficiency. Major constraints include limited sensitivity in paucibacterial samples, spectral interference from host matrices, difficulties in diagnosing polymicrobial infections, and gaps in reference databases for emerging pathogens. Direct MALDI-TOF MS is a transformative tool for rapid infection diagnosis. To fully realize its potential in routine practice, future advancements must integrate automated sample processing, enhance sensitivity via techniques like MALDI-2, and employ artificial intelligence for spectral analysis and resistance prediction. Overcoming these barriers will establish this technology as a cornerstone of rapid diagnostic pathways, improving patient outcomes and supporting antimicrobial stewardship.

OBJECTIVES:To investigate the immunopathogenic mechanisms of anti-N-methyl-D-aspartate receptor encephalitis (NMDAR-E) by characterizing the changes of immune cells in both peripheral blood (PB) and cerebrospinal fluid (CSF) of patients with NMDAR-E.METHODS:Cytology and flow cytometry were used to explore and compare different immunological parameters in PB and CSF of patients with NMDAR-E, viral encephalitis (VE) and healthy volunteers. Moreover, different models were established to assess the possibility of identifying NMDAR-E patients based on PB and CSF parameters.RESULTS:The neutrophil counts and monocyte-to-lymphocyte ratios (MLR) in PB are higher in NMDAR-E patients than in both VEs and controls (P < 0.001, respectively), while the percentages of CD3 + T, CD4 + T lymphocytes, and the leukocytes count in CSF were lower in NMDAR-Es than in VEs (P < 0.01, respectively). The higher percentages of CD8 + T cells in blood and CSF were both correlated with more severe NMDAR-E (P < 0.05, respectively). The poor neurological status group had significantly higher PB leukocytes but lower CSF leukocyte count (P < 0.05). Longitudinal observations in patients with NMDAR-E showed a decreasing trend of leukocyte count, neutrophils count, neutrophil-to-monocyte ratios (NMR), and neutrophil-to-lymphocyte ratios (NLR) with the gradual recovery of neurological function.CONCLUSIONS:The expression patterns of T lymphocyte subsets were different in patients with NMDAR-E and viral encephalitis. The changing trends of leukocyte and lymphocyte populations in peripheral blood and cerebrospinal fluid may provide clues for the diagnosis of different types of encephalitides, including NMDARE, and can be used as immunological markers to assess and predict the prognosis.

T cells are key drivers of the pathogenesis of autoimmune diseases by producing cytokines, stimulating the generation of autoantibodies, and mediating tissue and cell damage. Distinct mitochondrial metabolic pathways govern the direction of T-cell differentiation and function and rely on specific nutrients and metabolic enzymes. Metabolic substrate uptake and mitochondrial metabolism form the foundational elements for T-cell activation, proliferation, differentiation, and effector function, contributing to the dynamic interplay between immunological signals and mitochondrial metabolism in coordinating adaptive immunity. Perturbations in substrate availability and enzyme activity may impair T-cell immunosuppressive function, fostering autoreactive responses and disrupting immune homeostasis, ultimately contributing to autoimmune disease pathogenesis. A growing body of studies has explored how metabolic processes regulate the function of diverse T-cell subsets in autoimmune diseases such as systemic lupus erythematosus (SLE), multiple sclerosis (MS), autoimmune hepatitis (AIH), inflammatory bowel disease (IBD), and psoriasis. This review describes the coordination of T-cell biology by mitochondrial metabolism, including the electron transport chain (ETC), oxidative phosphorylation, amino acid metabolism, fatty acid metabolism, and one‑carbon metabolism. This study elucidated the intricate crosstalk between mitochondrial metabolic programs, signal transduction pathways, and transcription factors. This review summarizes potential therapeutic targets for T-cell mitochondrial metabolism and signaling in autoimmune diseases, providing insights for future studies.

Context Antinuclear antibodies (ANAs) against certain antigens are useful for identifying autoimmune disorders. Although new solid phase–based immunoassays have been developed for evaluating ANAs, the conventional line immunoassay (LIA) is commonly used in clinical practice. Objective To compare the clinical performance of 2 newly developed methods for detecting specific ANAs with LIA. Design Six hundred ninety-six serum samples were collected from 559 patients with autoimmune disease (AID) and 137 controls. The samples were screened by using the LIA, digital liquid chip method (DLCM), and chemiluminescent immunoassay (CLIA) for specific ANAs. The agreement across assays and the clinical performance of each assay in diagnosing ANA-associated rheumatic diseases (AARDs) were evaluated. Results Almost perfect agreement was observed among all assays for anti–centromere protein B (κ = 0.85–0.97), anti–ribosome P (κ = 0.85–0.88), anti–SSA 52 (κ = 0.86–0.89), and anti–SSA 60 (κ = 0.89–0.91); moderate to substantial agreement was detected for the autoantibodies against Sm, Jo-1, ribonucleoprotein, Scl-70, and SSB (κ = 0.55–0.80). LIA exhibited better sensitivity for diagnosing AARDs, while DLCM and CLIA demonstrated higher specificity. In the subset of AIDs, especially systemic lupus erythematosus, antibody positive percentages varied greatly between assays. Conclusions The 3 assays showed comparable qualitative agreement; however, the standardization of testing for ANAs remains challenging owing to intermanufacturer variations. Moreover, DLCM and CLIA exhibited better specificity in distinguishing non-AID individuals, whereas LIA was more sensitive in diagnosing AARDs.

Lead exposure causes great harm to the growth and development of infants. A simple and fast approach that can be conveniently used at home is thus needed for parents to screen the potential lead sources in their children's daily activities. Here, we developed a simple, fast, and sensitive gold nanoparticles (AuNPs)-based indicator for colorimetric Pb2+ detection. The method rationale was based on the higher affinity of Pb2+ to T30695 DNA over thioflavin T (ThT), as well as the stable and fast charge neutralization-induced assembly of AuNPs by ThT. To facilitate in-home monitoring, we arranged the reagents (AuNPs, DNA, ThT, and the buffer) and the required facilities (microplate and pipe) into a kit. Besides, the color change of the indicator AuNPs was monitored with a cell phone camera and processed with a self-developed APP. For samples closely related to children's daily activities, Pb2+ was successfully detected in saliva, sweat (simulated) and stomach fluid (simulated) extractions of water bottles, small benches, cushions, paint, lipstick, building blocks and toys. Therefore, continuous efforts are required for a lead-free life and such a kit can help the screening of lead-leaking clothing, food, shelter and toys for children.

Rheumatoid arthritis (RA) is a chronic inflammatory disease which is closely related to genetic background. Single-nucleotide polymorphisms (SNPs) have been found to play an important role in the development of RA. This study intends to investigate the links between gene polymorphisms in the interleukin-23 receptor (IL23R) and interleukin 17A (IL17A) and susceptibility to RA in the Western Chinese Han population. Four SNPs (rs6693831 T > C, rs1884444 G > T, and rs7517847 T > G in IL23R gene, and rs2275913 G > A in IL17A gene) were genotyped in 246 RA patients and 362 healthy controls by high resolution melting analysis. The comparative analyses among genotype distributions, clinical indicators, and IL-17A and IL-23R levels in RA patients were also performed. The study revealed that the SNP rs6693831 and rs1884444 of IL23R had a significant association with RA susceptibility. The frequencies of rs6693831 genotype CC and allele C were significantly higher in the RA group and associated with higher RA risk compared with genotype TT and allele T (OR = 7.797, 95% confidence interval [CI] = 4.072-14.932 and OR = 5.984, 95%CI = 3.190-11.224, respectively). The TT genotype of rs1884444 appeared to decrease the RA risk compared with the GG genotype (OR = .251, 95%CI = .118-.536). The genotype CC and allele C of rs6693831 and the genotype GG and allele G of rs1884444 may be risk factors for RA. IL23R gene polymorphisms may be involved in the risk of RA susceptibility in the Western Chinese Han population.