Open AccessDepression of cellular‐mediated immunity in systemic lupus erythematosus
Author(s) -
Julian Rosenthal C.,
Franklin Edward C.
Publication year - 1975
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780180303
Subject(s) - medicine , immunology , cellular immunity , prednisone , antigen , stimulation , depression (economics) , in vitro , lupus erythematosus , delayed hypersensitivity , immunity , lymphocyte , immune system , biology , antibody , biochemistry , economics , macroeconomics
Cellular‐mediated immunity was examined in 6 consecutive patients with active SLE, 6 patients with low active SLE, 6 patients with DLE, 8 patients with other collagen diseases, and 9 healthy controls. The following parameters were measured: delayed hypersensitivity, in vitro lymphocyte blast transformation, and MIF production after stimulation with five common antigens, DNA, and two nonspecific mitogens (PHA, PWM). The 6 active SLE patients were anergic and had a markedly depressed response in vitro to the specific antigens and PWM ( P < 0.001 ). When CMI was retested in 5 patients as early as 5 days after the start of prednisone (60 mg/day), the results were significantly improved in 4 who also improved clinically, and they remained unchanged in a fifth patient who failed to improve. There was a less marked impairment of CMI among the low active SLE group, whereas the DLE and OCD patients did not differ significantly from the control subjects. DNA did not cause significant stimulation of blast transformation in any of the study groups.