Background Cell division control protein 42 (CDC42) is reported to be involved in multiple inflammation processes by regulating T cell differentiation, maintaining immune cell homeostasis, and altering their function, while no relevant studies explored its clinical role in patients with rheumatoid arthritis (RA). Therefore, this study aimed to explore the correlation of CDC42 with Th1 and Th17 cells and its association with disease risk, activity, and treatment outcomes of RA. Methods After the enrollment of 95 active RA patients and 50 healthy subjects (HC), their CDC42, Th1 cells, and Th17 cells were assayed by RT-qPCR and flow cytometry, accordingly. For RA patients only, CDC42 was also detected at W6, and W12 after treatment. The treatment response and remission status were evaluated at W12. Results Compared to HC, CDC42 was reduced (P < 0.001), while Th1 cells (P = 0.021) and Th17 cells (P < 0.001) were increased in RA patients. Besides, CDC42 was negatively correlated with Th17 cells (P < 0.001), erythrocyte sedimentation rate (ESR) (P = 0.012), C-reactive protein (P = 0.002), and disease activity score in 28 joints (DAS28) (P = 0.007), but did not relate to Th1 cells or other disease features (all P > 0.05) in RA patients. Furthermore, CDC42 was elevated during treatment in RA patients (P < 0.001). Moreover, CDC42 increment at W12 correlated with treatment response (P = 0.004). Besides, CDC42 elevation at W0 (P = 0.038), W6 (P = 0.001), and W12 (P < 0.001) also linked with treatment remission. Conclusion CDC42 has the potential to serve as a biomarker to monitor disease activity and treatment efficacy in patients with RA.

Background Mucosa‐associated lymphoid tissue lymphoma translocation protein 1 (MALT1) correlates with treatment outcomes in inflammatory bowel disease and rheumatoid arthritis (RA). This study aimed to further evaluate the MALT1 longitudinal change and its relationship with tumor necrosis factor inhibitors (TNFi) response in RA patients. Methods Seventy‐one RA patients receiving TNFi [etanercept ( n = 42) or adalimumab ( n = 29)] were enrolled. MALT1 was detected by RT‐qPCR in peripheral blood samples of RA patients before treatment (W0), at week (W)4, W12, and W24 after treatment. RA patients were divided into response/non‐response, remission/non‐remission patients according to their treatment outcome at W24. Meanwhile, MALT1 was also detected by RT‐qPCR in 30 osteoarthritis patients and 30 healthy controls (HCs). Results Mucosa‐associated lymphoid tissue lymphoma translocation protein 1 was elevated in RA patients compared with HCs ( Z =−6.392, p < 0.001) and osteoarthritis patients ( Z = −5.020, p < 0.001). In RA patients, MALT1 was positively correlated with C‐reactive protein ( r s = 0.347, p = 0.003), but not other clinical characteristics, treatment history, or current TNFi category. Meanwhile, MALT1 decreased from W0 to W12 in total RA patients ( x 2 = 86.455, p < 0.001), etanercept subgroup ( x 2 = 46.636, p < 0.001), and adalimumab subgroup ( x 2 = 41.291, p < 0.001). Moreover, MALT1 at W24 ( p = 0.012) was decreased in response patients compared with non‐response patients; MALT1 at W12 ( p = 0.027) and W24 ( p = 0.010) were reduced in remission patients than non‐remission patients. In etanercept subgroup, MALT1 at W24 ( p = 0.013) was decreased in response patients compared with non‐response patients. In adalimumab subgroup, MALT1 at W24 ( p = 0.015) was lower in remission patients than non‐remission patients. Conclusion Mucosa‐associated lymphoid tissue lymphoma translocation protein 1 reduction after treatment is associated with response and remission to TNFi in RA patients.

No abstract