Abstract

Purified blood monocytes from patients with rheumatoid arthritis (RA) were significantly less capable of presenting purified protein derivative of tuberculin (PPD) to autologous lymphocytes than monocytes from patients with osteoarthritis, degenerative spine diseases, or healthy controls. Since lymphocytes from RA patients exhibited a normal response to soluble PPD or concanavalin A, the lowered T-cell reactivity had to be attributed to a diminished antigen-presenting capacity of monocytes. Several reasons may be responsible for this altered monocyte function in rheumatoid arthritis: a shift of monocytes to subpopulations expressing less Ia-like antigens, an inherent monocyte disorder, or a “preactivation” of monocytes associated with a reduced antigen-presenting capacity.

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