Myalgic Encephalopathy\/Chronic Fatigue Syndrome (ME\/CFS) is a disease of unknown etiology.<\/p>\n
We have previously suggested clinical benefit from B-cell <\/a>depletion using the monoclonal anti-CD20 antibody rituximab in a randomized and placebo-controlled study. Prolonged responses were then demonstrated in an open-label phase-II study with maintenance rituximab treatment.<\/p>\n Using blood samples from patients in the previous two clinical trials, we investigated quantitative changes in T-lymphocyte subsets, in immunoglobulins, and in serum levels of two B-cell regulating cytokines during follow-up. B-lymphocyte activating factor of the tumor necrosis family (BAFF) in baseline serum samples was elevated in 70 ME\/CFS patients as compared to 56 healthy controls (p=0.011).<\/p>\n There were no significant differences in baseline serum BAFF levels between patients with mild, moderate, or severe ME\/CFS, or between responders and non-responders to rituximab. A proliferation-inducing ligand (APRIL) serum levels were not significantly different in ME\/CFS patients compared to healthy controls at baseline, and no changes in\u00a0serum levels were seen during follow-up.<\/p>\n Immunophenotyping<\/a> of peripheral blood T-lymphocyte subsets and T-cell activation markers at multiple time points during follow-up showed no significant differences over time, between rituximab and placebo groups, or between responders and non-responders to rituximab. Baseline serum IgG levels were significantly lower in patients with subsequent response after rituximab therapy compared to non-responders (p=0.03).<\/p>\n In the maintenance study, slight but significant reductions in mean serum immunoglobulin levels were observed at 24 months compared to baseline; IgG 10.6-9.5 g\/L, IgA 1.8-1.5 g\/L, and IgM 0.97-0.70 g\/L.<\/p>\n Although no functional assays were performed, the lack of significant associations of T- and NK-cell subset numbers with B-cell depletion, as well as the lack of associations to\u00a0clinical responses, suggest that B-cell regulatory effects on T-cell or NK-cell subsets are not the main mechanisms for the observed improvements in ME\/CFS symptoms observed in the two previous trials.<\/p>\n The modest increase in serum BAFF levels at baseline may indicate an activated B-lymphocyte system in a subgroup of ME\/CFS patients.<\/p>\n Serum BAFF and APRIL Levels, T-Lymphocyte Subsets, and Immunoglobulins after B-Cell Depletion Using the Monoclonal Anti-CD20 Antibody Rituximab in Myalgic Encephalopathy\/Chronic Fatigue Syndrome<\/a> by Sigrid Lunde, Einar K. Kristoffersen, Dipak Sapkota, Kristin Risa, Olav Dahl, Ove Bruland, Olav Mella, Oystein Fluge in<\/span> PLoS One<\/em> vol. 11, #8,\u00a0August 18, 2016<\/p>\n","protected":false},"excerpt":{"rendered":" Research abstract: Myalgic Encephalopathy\/Chronic Fatigue Syndrome (ME\/CFS) is a disease of unknown etiology. We have previously suggested clinical benefit from B-cell depletion using the monoclonal anti-CD20 antibody rituximab in a randomized and placebo-controlled study. Prolonged responses were then demonstrated in … Continue reading