IL-4 down-regulates the surface expression of CD5 on B cells and inhibits spontaneous immunoglobulin and IgM-rheumatoid factor production in patients with rheumatoid arthritis

Open Access
Publisher Website
Google Scholar
Abstract
There is evidence to suggest that CD5+ B cells may be associated with autoimmunity, e.g. they are increased in patients with rheumatoid arthritis (RA). In this study, we found that the expression of CD5 on RA B cells increased spontaneously, following culture for up to 4 days in vitro in the absence of T cells, supporting the idea that the CD5+ B cell possesses distinctive features. The spontaneous increase of CD5 expression was down‐regulated by recombinant IL‐4 (rIL‐4). Other cytokines studied (rIL‐1α, rIL‐2, rIL‐5, rIL‐6) did not alter CD5 expression. Studies of antibody production showed that rIL‐4 could reduce spontaneous production of total IgG and IgM in non‐stimulated RA T plus B cell cultures. Spontaneous production of IgM rheumatoid factor (IgM‐RF), measured by a newly developed avidin‐biotin complex ELISA, was also reduced by rIL‐4. Furthermore, rIL‐4 reduced the increase in IgM‐RF production observed on stimulation with Staphylococcus aureus Cowan I (SAC) or pokeweed mitogen (PWM). Thus, IL‐4 might act as a regulator of the development of abnormal B cell differentiation in patients with RA.