Monocytes in rheumatoid arthritis. Regulatory, effector, and phenotypic properties.

We reported that rheumatoid arthritis (RA) blood mononuclear cells (MNC) secreted less Ig and IgM rheumatoid factor (RF) than synovial cells. Since antibody elaboration is partly monocyte dependent, we compared regulatory, effector, and phenotypic properties of monocytes from 31 patients with RA with those of 21 normal subjects. RA IgG and IgM elaboration was less than normal. Monocyte, T or B cell numbers were comparable in RA and normal MNC and monocyte enriched/depleted preparations. RA and normal Ig production were monocyte dependent and this differed for IgG and IgM for RA and normals. IgM RF elaboration by stimulated RA MNC was also monocyte dependent and addition of normal monocytes/monocyte culture supernatants to RA monocyte depleted cultures and vice versa had inconsistent effects. RA MNC (Ficoll-Hypaque) phagocytosis was less than normal; killing (acridine orange fluorescent microscopy) was not. RA synovial monocyte phagocytosis - but not killing was also reduced. MNC from RA patients and normals contained similar numbers of monocytes; RA monocyte enriched populations (Percoll) showed less phagocytosis than normal; with similar killing. RA phagocytosis was reduced at 1,2,3,4 and 5 h and differed from normal at 3 and 5 h. Different sera - FCS, autologous, normal, RA - exhibited inconsistent effects on phagocytosis. RA and normal neutrophil phagocytosis and killing were comparable. Lastly, RA monocyte enriched preparations contained populations of OKM1, OKM3, OKM5, OKM6, Leu M1, Leu M2, Leu M3, and HLA-DR-positive cells (FACS analysis) comparable with normals. Regulatory and effector but not phenotypic properties of RA blood monocytes differed from normal and may contribute to inappropriate autoantibody production and chronic inflammation.