We investigated whether mononuclear cells (MNC) from patients with seronegative rheumatoid arthritis (SNRA) are able to produce rheumatoid factor (RF) in response to lectin stimulation, Staphylococcus aureus Cowan I (SAC) or pokeweed mitogen (PWM), and also we investigated the role of CD5+ B cells in the pathogenesis of in vitro IgM RF production.
IgM RF production was measured by enzyme linked immunosorbent assay and CD5+ B cells by flow cytometry. Also, the effects of monocyte depletion and the inhibition of prostaglandin (PG) were compared in SNRA, seropositive RA (SPRA) and healthy controls.
Peripheral blood MNC of patients with SNRA were able to produce the same amount of IgM RF as patients with SPRA following stimulation and SAC. CD5+ B cells also increased in patients with SNRA as well as patients with SPRA compared to healthy controls. However, a definite contribution of the CD5+ B cells to SAC-induced IgM RF production could not be demonstrated. The role of macrophage and PG on in vitro IgM RF synthesis were insignificant.
MNC of patients with SNRA were able to produce IgM and IgG RF in response to SAC stimulation as well as that of the healthy controls. However, we could not find a significant role of CD5+ B cells and monocytes on in vitro IgM RF synthesis by MNC of patients with SNRA.