Defective Phagocytosis by Synovial Fluid and Blood Polymorphonuclear Leucocytes in Patients with Rheumatoid Arthritis. I. The Nature of the Defect
*Correspondence: Dr J. M. A. Wilton, Department of Oral Immunology and Microbiology, Guy's Hospital Medical and Dental Schools, London SE1 9RT
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Abstract |
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In a series of thirty-seven patients with rheumatoid arthritis (RA), 50% showed a defect of phagocytosis of Candida albicans by synovial fluid polymorphonuclear leucocytes (SF-PMN) and 40% yielded a defect in peripheral blood (PB-PMN). There was a positive correlation between the defective phagocytosis of SF-PMN and PB-PMN suggesting that defective PB-PMN migrate into the synovial fluid. The defect was associated with the lack of a functional C3b receptor on SF-PMN in 64% of patients and on PB-PMN in 40% of patients. SF-PMN or PB-PMN contained intracellular IgG, IgM and C3 in some patients but the presence of these factors could not be correlated with defective phagocytosis of either cell population. There was no correlation between phagocytosis and the differential agglutination test (DAT) ratio of either serum or synovial fluid. The killing of Candida by SF-PMN and BP-PMN was normal. The results could explain the increased susceptibility to joint infection of patients with RA.