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Rheumatoid arthritis (RA) is a chronic autoimmune disease that gradually limits physical function and decreases quality of life (QOL). We evaluated an mHealth‐based self‐management program to help patients with RA improve their physical and psychological health, self‐efficacy, physical activity, and QOL. The sample included 73 experimental and 69 control participants. A pilot randomized controlled design was employed to identify the effectiveness of an 8‐week mHealth‐based self‐management program, which comprised educational modules regarding disease management and exercise, cognitive training, and motivational support through mobile messages and periodic phone calls. Knowledge of the health effects of RA, disease activity, perceived health, depression, self‐efficacy for controlling symptoms, physical activity, and QOL were evaluated pre‐ and postintervention and after the 4‐week follow‐up period. This pilot study indicates that the mHealth‐based program for people with RA is feasible. The mHealth self‐management program improved patients' knowledge of RA, depression, self‐efficacy for controlling symptoms, physical activity, and perceived health; however, disease activity and QOL did not significantly change. This pilot study demonstrates the potential of mHealth intervention as an effective program for strengthening self‐management capacities in patients with RA. Trial Registration: KCT0007523 [ABSTRACT FROM AUTHOR]

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease caused by autoantibodies. Serum samples from patients with SLE (n = 10) were compared with those from normal controls (NCs, n = 5) using 21K protein chip analysis to identify a biomarker for SLE, revealing 63 SLE-specific autoantibodies. The anti-chaperonin-containing t-complex polypeptide-1 (TCP1) antibody exhibited higher expression in patients with SLE than in NCs. To validate the specificity of the anti-TCP1 antibody in SLE, dot blot analysis was conducted using sera from patients with SLE (n = 100), rheumatoid arthritis (RA; n = 25), Behçet's disease (BD; n = 28), and systemic sclerosis (SSc; n = 30) and NCs (n = 50). The results confirmed the detection of anti-TCP1 antibodies in 79 of 100 patients with SLE, with substantially elevated expression compared to both NCs and patients with other autoimmune diseases. We performed an enzyme-linked immunosorbent assay to determine the relative amounts of anti-TCP1 antibodies; markedly elevated anti-TCP1 antibody levels were detected in the sera of patients with SLE (50.1 ± 17.3 arbitrary unit (AU), n = 251) compared to those in NCs (33.9 ± 9.3 AU), RA (35 ± 8.7 AU), BD (37.5 ± 11.6 AU), and SSc (43 ± 11.9 AU). These data suggest that the anti-TCP1 antibody is a potential diagnostic biomarker for SLE. [ABSTRACT FROM AUTHOR]

Arterial macrophage cholesterol accumulation and impaired cholesterol efflux lead to foam cell formation and the development of atherosclerosis. Modified lipoproteins interact with toll-like receptors (TLR), causing an increased inflammatory response and altered cholesterol homeostasis. We aimed to determine the effects of TLR antagonists on cholesterol efflux and foam cell formation in human macrophages. Stimulated monocytes were treated with TLR antagonists (MIP2), and the cholesterol efflux transporter expression and foam cell formation were analyzed. The administration of MIP2 attenuated the foam cell formation induced by lipopolysaccharides (LPS) and oxidized low-density lipoproteins (ox-LDL) in stimulated THP-1 cells (p < 0.001). The expression of ATP-binding cassette transporters A (ABCA)-1, ABCG-1, scavenger receptor (SR)-B1, liver X receptor (LXR)-α, and peroxisome proliferator-activated receptor (PPAR)-γ mRNA and proteins were increased (p < 0.001) following MIP2 administration. A concentration-dependent decrease in the phosphorylation of p65, p38, and JNK was also observed following MIP2 administration. Moreover, an inhibition of p65 phosphorylation enhanced the expression of ABCA1, ABCG1, SR-B1, and LXR-α. TLR inhibition promoted the cholesterol efflux pathway by increasing the expression of ABCA-1, ABCG-1, and SR-B1, thereby reducing foam cell formation. Our results suggest a potential role of the p65/NF-kB/LXR-α/ABCA1 axis in TLR-mediated cholesterol homeostasis. [ABSTRACT FROM AUTHOR]

Aim: This post hoc analysis evaluated the efficacy and safety of intravenous belimumab 10 mg/kg in the South Korean subgroup of patients with systemic lupus erythematosus (SLE) enrolled in the North East Asia (NEA) study (GSK Study BEL113750; NCT01345253). Methods: NEA was a double‐blind, placebo‐controlled, randomized Phase 3 trial. Patients with active, autoantibody‐positive SLE were randomized 2:1 to belimumab or placebo plus standard therapy administered on Days 0, 14, and 28, and then every 28 days up to Week 48. The primary efficacy endpoint in this analysis was SLE Responder Index 4 (SRI‐4) response rate at Week 52, defined as the proportion of patients achieving a ≥4‐point reduction in Safety of Estrogens in Lupus Erythematosus National Assessment‐SLE Disease Activity Index (SELENA‐SLEDAI) score, no worsening (<0.3 increase from baseline) in Physician Global Assessment, no new British Isles Lupus Assessment Group (BILAG) A domain and <2 new BILAG B domain scores. Results: Among 100 South Korean patients enrolled in NEA, 54/66 (81.8%) belimumab‐ and 24/34 (70.6%) placebo‐treated patients completed the double‐blind phase. Significantly more belimumab‐ than placebo‐treated patients achieved SRI‐4 response at Week 52 (n = 35/66, 53.0% vs. n = 8/34, 23.5%; odds ratio [OR; 95% confidence interval (CI)]: 3.67 [1.45, 9.28]; p =.0061). The proportion of patients experiencing ≥1 adverse event was similar between groups (belimumab: n = 60/66, 90.9% vs. placebo: n = 31/34, 91.2%). No new safety signals emerged in this subgroup analysis. Conclusion: Belimumab was efficacious for the treatment of SLE and well tolerated among the South Korean subgroup of patients from the NEA study. [ABSTRACT FROM AUTHOR]

Background: Seasonal variation and sunlight exposure can impact serum vitamin D levels, potentially influencing lupus symptoms. We investigated seasonal vitamin D levels and their correlation with clinical manifestations and disease activity in systemic lupus erythematosus (SLE). Methods: Serum 25(OH) vitamin D3 (25(OH)D3) levels were categorised as deficient (25(OH)D3 < 10 ng/mL), insufficient (10–30 ng/mL) and sufficiency (>30 ng/mL) in participants analysed in winter (n = 407) and summer (n = 377). Logistic regression analysis was performed to assess the impact of vitamin D levels on achieving a lupus low disease activity state (LLDAS), stratified by season. Results: The mean serum 25(OH)D3 levels differed significantly between the winter and summer measurement groups (22.4 vs. 24.2 ng/mL; p =.018). The prevalences of vitamin D deficiency, insufficiency and sufficiency in the winter group were 12.8%, 66.6% and 20.6%, respectively, compared with 4.5%, 67.9% and 27.6% in the summer group. Achieving LLDAS was highest in the vitamin D sufficiency group (winter: 56.6%, summer: 55%) and lowest in the vitamin D deficiency group (winter: 15.4%, summer: 13.6%), with significant differences (all p <.001). Multivariate analysis identified SLE disease activity index ≤4, normal anti‐double‐stranded DNA and vitamin D sufficiency as significant factors for achieving LLDAS in both seasons. Conclusions: Sufficient vitamin D levels are important for achieving LLDAS in patients with SLE during winter and summer. Therefore, physicians should pay attention to the adequacy of vitamin D levels and consider recommending vitamin D supplementation for patients with vitamin D insufficiency. [ABSTRACT FROM AUTHOR]

Communication between CD4 T cells and cognate B cells is key for the former to fully mature into germinal center–T follicular helper (GC-TFH) cells and for the latter to mount a CD4 T cell–dependent humoral immune response. Although this interaction occurs in a B:T synapse–dependent manner, how CD4 T cells transcriptionally regulate B:T synapse formation remains largely unknown. Here, we report that Mef2d, an isoform of the myocyte enhancer factor 2 (Mef2) transcription factor family, is a critical regulator of this process. In CD4 T cells, Mef2d negatively regulates expression of Sh2d1a, which encodes SLAM-associated protein (SAP), a critical regulator of B:T synapses. We found that Mef2d regulates Sh2d1a expression via DNA binding–dependent transcriptional repression, inhibiting SAP-dependent B:T synapse formation and preventing antigen-specific CD4 T cells from differentiating into GC-TFH cells. Mef2d also impeded IL-21 production by CD4 T cells, an important B cell help signaling molecule, via direct repression of the Il21 gene. In contrast, CD4 T cell–specific disruption of Mef2d led to a substantial increase in GC-TFH differentiation in response to protein immunization, concurrent with enhanced SAP expression. MEF2D mRNA expression inversely correlates with human systemic lupus erythematosus (SLE) patient autoimmune parameters, including circulating TFH–like cell frequencies, autoantibodies, and SLEDAI scores. These findings highlight Mef2d as a pivotal rheostat in CD4 T cells for controlling GC formation and antibody production by B cells. SAP and the synapse: The immune synapse promotes stable interactions between CD4 T cells with antigen presenting cells. There is a requirement for the adaptor protein SAP in the formation of the B:T immune synapse; however, it is unknown how the gene encoding SAP, Sh2d1a, is regulated in CD4 T cells. Kim et al. studied the role of the transcription factor Mef2d in transcriptional regulation of Sh2d1a and subsequent immune synapse formation. They found that Mef2d directly repressed Sh2d1a, inhibiting immune synapse formation and GC-TFH differentiation. Mef2d also directly repressed Il21, resulting in impaired germinal center formation and antibody production after immunization. Furthermore, MEF2D expression inversely correlated with autoimmunity in humans. Together, these findings suggest that Mef2d functions as a checkpoint to restrain inappropriate GC-TFH differentiation and humoral immunity. —HMI [ABSTRACT FROM AUTHOR]

Objective: Pain is a significant and debilitating symptom of rheumatoid arthritis (RA) that significantly affects the quality of life and functional ability of patients. In the present study, we examined the association between pain variables and disease activity markers in patients with RA., Methods: We enrolled 133 patients with RA and assessed their clinical characteristics, socioeconomic and psychological factors, and pain measures. The psychological factors assessed included depressive symptoms and pain catastrophizing., Results: The study cohort comprised predominantly female patients with RA with an average age of 55.5±10.1 years. Depressive symptoms had a mean score of 5.83±4.71, while pain catastrophizing had an average score of 14.36±10.70. The mean scores for pain intensity, and pain interference, were 2.98±1.75 and 19.54±16.17, respectively, with significant positive correlations observed with depressive symptoms. Hemoglobin and hematocrit levels were negatively correlated with pain intensity. Multivariable linear regression analysis revealed significant associations between depressive symptoms and pain intensity, catastrophizing, and interference. Other factors associated with pain intensity included tender joint count. Pain catastrophizing was associated with education and economic status. Pain interference was associated with sex and economic status., Conclusion: This study shows the influence of disease-related indicators and psychological factors on pain in patients with RA, with depressive symptoms playing a crucial role in predicting pain experience. Effective pain management strategies for RA should include the management of depressive symptoms, in addition to addressing disease-related indicators., Competing Interests: CONFLICT OF INTEREST No potential conflict of interest relevant to this article was reported., (Copyright © 2025 by The Korean College of Rheumatology. All rights reserved.)

Objectives: This study aimed to identify the risk factors associated with overall adverse events (AEs) and infections in patients with rheumatoid arthritis (RA) and comorbid interstitial lung disease (ILD), receiving biologic or targeted synthetic disease-modifying anti-rheumatic drugs (b/tsDMARDs), using data from the Korean College of Rheumatology Biologics registry., Methods: We analysed data from a cohort of 2,266 adult patients with RA who received b/tsDMARDs, including 169 patients with comorbid ILD. We identified the risk factors for overall AEs and infections in both the all RA group and the subgroup of patients with RA-ILD and investigated the impact of infections on mortality in patients with RA-ILD., Results: Among all patients with RA, 45.7% withdrew b/tsDMARDs, whereas among those with RA-ILD, a higher proportion of 57.4% withdrew their treatment regimen. The main reason for withdrawing b/tsDMARDs in the RA-ILD group was AEs, with infections accounting for the largest proportion of reported AEs. In multivariable analysis of the risk factors for overall AEs and infections in the RA-ILD group, older age was identified as a risk factor for overall AEs (odds ratio [OR], 3.01; p=0.014), and only a current smoking status was identified as a risk factor for infections (OR, 2.11; p=0.035)., Conclusions: Patients with RA-ILD exhibited a higher rate of b/tsDMARDs withdrawal due to overall AEs and infections than those with RA without ILD. In the RA-ILD group, older age was identified as a risk factor for overall AEs, whereas a current smoking status was identified as a risk factor for infections.