ABSTRACT
BACKGROUND: Cognitive behavioral therapy (CBT) has proven useful in treating fibromyalgia, depression, and anxiety. Computerized delivery of CBT allows increased access to such therapy. This study assessed the effect of internet-based CBT on Fibromyalgia Impact Questionnaire (FIQ) composite scores and tender point assessments. METHODS: This 12-week randomized controlled trial included patients ≥18 years of age with 1990 American College of Rheumatology criteria for fibromyalgia and mild to moderate depression and anxiety. A total of 56 subjects were randomized into either a 6-week internet-based CBT group (MoodGYM) or a control group (standard care). We evaluated patients in both groups at 1-, 6-, and 12-week follow-up. The primary outcome measure was change in FIQ composite score. A secondary outcome measure was change in tender point assessment. RESULTS: The mean age of study participants was 55 years, and 88% were female. Mean FIQ scores were significantly lower in the MoodGYM group compared to the control group (P<0.05 for group differences at 6 and 12 weeks). Mean tender point scores were also significantly lower in the MoodGYM group (P<0.001 at 6 and 12 weeks). We found no significant difference in the FIQ scores across the 3 timepoints in the MoodGYM group, but tender points showed a significant negative trend from baseline to 12-week follow-up. CONCLUSION: Patients in the internet-based MoodGYM CBT program had lower FIQ and tender point scores at 6- and 12-week follow-up. Internet-based CBT could be beneficial in the treatment of mild to moderate depression and anxiety in patients with fibromyalgia by allowing increased access to CBT.
ABSTRACT
BACKGROUND: Autoimmune diseases (such as systemic lupus erythematosus, rheumatoid arthritis, type 1 diabetes, etc) are characterized by the production of autoantibodies against one's own cell components, resulting in the dysfunction of normal organs. At present, therapies for autoimmune diseases involve a variety of nonspecific antiinflammatory and immunosuppressive agents with significant side effects. Current studies have suggested that the germinal center (GC) may be the pathogenic hot spot for the production of autoantibodies in autoimmune disease. Events occurring in the GC-such as the selection of high-affinity B cells, proliferation of B cells, and differentiation of B cells into plasma cells-all depend on T cells. Follicular helper T (Tfh) cells are a recently identified T-cell subset, named for their location in GCs. Tfh cells are characterized by their signature transcription factor (B-cell lymphoma 6), surface molecules (CD40 ligand, chemokine [C-X-C] receptor 5, inducible T-cell costimulator, programmed cell death protein-1, etc), and cytokines (interleukin [IL]-21, IL-6, IL-10, etc). Through these signals, Tfh cells help B cells form GCs and drive B cells to differentiate into memory B cells and plasma cells that produce antibodies. However, uncontrolled generation of Tfh cells in the GCs or peripherals could lead to autoimmunity. Recent studies from our group and others have shown that Tfh cells are expanded in the peripheral blood of patients and in the lymphoid tissues of mice with lupus or rheumatoid arthritis and play an important role in promoting pathogenic autoantibody production. METHODS: In this review, we summarize the latest immunologic findings regarding the characteristics and development of Tfh cells, their relation to other CD4(+) T-cell subsets, and the function of Tfh cells in normal immune response and autoimmune diseases. CONCLUSION: A clear understanding of the mechanisms of Tfh cell-mediated immunity and pathology may lead to the development of novel therapeutic targets in autoimmune diseases.
