Nonaka S, Yasuda M, Nobunaga M
Department of Clinical Immunology, Kyushu University, Beppu Oita, Japan.
J Rheumatol. 1993 Sep;20(9):1478-84.
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.
我们研究了血清阴性类风湿关节炎（SNRA）患者的单核细胞（MNC）在受到凝集素刺激、金黄色葡萄球菌Cowan I（SAC）或商陆有丝分裂原（PWM）刺激时是否能够产生类风湿因子（RF），并且我们还研究了CD5⁺ B细胞在体外IgM RF产生的发病机制中的作用。
通过酶联免疫吸附测定法测量IgM RF的产生，通过流式细胞术检测CD5⁺ B细胞。此外，还比较了SNRA、血清阳性类风湿关节炎（SPRA）患者和健康对照中单核细胞清除和前列腺素（PG）抑制的效果。
SNRA患者的外周血MNC在受到刺激和SAC刺激后能够产生与SPRA患者相同量的IgM RF。与健康对照相比，SNRA患者以及SPRA患者的CD5⁺ B细胞也有所增加。然而，无法证明CD5⁺ B细胞对SAC诱导的IgM RF产生有明确贡献。巨噬细胞和PG对体外IgM RF合成的作用不显著。
SNRA患者的MNC在受到SAC刺激时能够产生IgM和IgG RF，与健康对照一样。然而，我们未发现CD5⁺ B细胞和单核细胞在SNRA患者的MNC体外IgM RF合成中起显著作用。
