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Direct Demonstration of Immunoregulatory T‐Cell Defects in Patients with Systemic Lupus Erythematosus
Author(s) -
KOIDE J.,
TAKANO M.,
TAKEUCHI T.,
HOSONO O.,
AMANO K.,
HOMMA M.,
ABE T.
Publication year - 1986
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1986.tb03076.x
Subject(s) - antibody , suppressor , immunology , anti nuclear antibody , effector , cell , t cell , b cell , medicine , inducer , disease , systemic lupus erythematosus , biology , immune system , autoantibody , biochemistry , genetics , cancer , gene
The present study was undertaken to determine directly whether immunoregulatory T cells have a defective suppressor function in patients with systemic lupus erythematosus (SLE), and whether anti‐T‐cell antibodies are essential for immunoregulatory T‐cell defects. Peripheral blood T cells and T‐cell subsets were determined in 52 SLE patients. The ratio of T4 to T8 cells was distributed over a wider range in patients with SLE than in the controls. Patients with SLE were divided into three groups (low, normal and high) by the T4/T8 ratio. Lymphocytes from 12 SLE patients (7 with low and 5 with high T4/T8 ratios) were studied extensively. Their disease was inactive or in remission, Anti‐T‐cell antibodies were not detected, and yet the patients had immunological abnormalities characterized by the presence of antinuclear antibodies and hypergammaglobulinaemia. The SLE patients with high T4/T8 ratios had a decreased number of'T8 cells, and defective suppressor‐effector cells. In contrast, patients with low T4/T8 ratios had decreased T4 cells and/or increased T8 cells, and defective suppressor‐inducer cells. Two patients with low T4/T8 ratios had both suppressor‐effector and suppressor‐inducer cell defects. These results indicate that immunuregulaiory circuits in SLE patients are heterogeneous and that immunoregulatory defects exist even when the disease is inactive or in remission. Anti‐T‐cell antibodies were not essential for such immunoregulatory defects. Thus, immunoregulatory T‐cell defects and the development of SLE may be independent conditions due to other unknown causes.