Open AccessSuppression of the normal autologous mixed leukocyte reaction by sera from patients with systemic lupus erythematosus
Author(s) -
Hahn Bevra H.,
Pletscher L. Susan,
Muniain Miguel,
Macdermott Richard P.
Publication year - 1982
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780250404
Subject(s) - immunology , peripheral blood mononuclear cell , exacerbation , mixed lymphocyte reaction , medicine , antibody , lupus erythematosus , null cell , b cell , systemic lupus erythematosus , t cell , cell culture , biology , immune system , in vitro , disease , biochemistry , genetics
Sera from 15 patients with active systemic lupus erythematosus and 7 patients with inactive lupus were added to normal autologous mixed leukocyte reaction (MLR) cultures. Twelve of the 22 sera reduced autologous T cell proliferative responsiveness to B plus null (B+N) cells or macrophages by 50% or more. This inhibition correlated with defective autologous MLR in fresh mononuclear cells from those patients. When normal responding and stimulating cell populations were preincubated with suppressive lupus sera, then added to autologous MLR cultures that contained normal serum, proliferative responses were also reduced; inhibitors are directed against participating mononuclear cell subpopulations. The suppressive serum factors were directed variously against monocyte/macrophage (MΦ), B+N, or T cell populations; MΦ/T interactions were suppressed most frequently. The inhibitors were not removed by high‐speed centrifugation or by depletion of antibodies to DNA, and they did not correlate with the presence of lymphocytotoxic antibodies. The presence of serum inhibitors of normal MΦ/T and B+N/T autologous MLR may be an immunologic abnormality important in the initiation, perpetuation, or exacerbation of systemic lupus erythematosus.