Open AccessEnhancement of IL‐1, IL‐2 production and IL‐2 receptor generation in patients with acute rheumatic fever and active rheumatic heart disease; a prospective study
Author(s) -
MORRIS K.,
MOHAN C.,
WAHI P. L.,
ANAND I. S.,
GANGULY N. K.
Publication year - 1993
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1993.tb05920.x
Subject(s) - peripheral blood mononuclear cell , immunology , il 2 receptor , phytohaemagglutinin , medicine , interleukin 2 , cd8 , immune system , rheumatic fever , cytotoxic t cell , t cell , biology , in vitro , biochemistry
SUMMARY In a prospective study, patients with quiescent rheumatic heart disease (CRHD), streptococcal pharyngitis (SP) and healthy normal subjects produced comparable amounts of IL‐1 and IL‐2, but acute rheumatic fever (ARF) patients produced significantly elevated amounts of IL‐1 and IL‐2 at all intervals up to 48 weeks. In active rheumatic heart disease (ARHD), IL‐1 activity returned to within normal range at 48 weeks, but IL‐2 activity remained persistently elevated compared with CRHD, SP and healthy age‐ and sex‐matched volunteers. CD4 + T lymphocytes were significantly increased in the peripheral blood of ARF and ARHD patients. The amount of IL‐2 produced by ARF and ARHD patients correlated with the percentage of helper T lymphocytes (CD4 + cells) but not with the percentage of suppressor/cytotoxic T lymphocytes (CD8 + cells). Moreover, pre‐ and post‐phytohaemagglutinin (PHA)‐stimulated peripheral blood mononuclear cell (PBMC) cultures from ARF and ARHD patients contained higher proportions of IL‐2R + (CD25 + ) cells than those from patients with SP, CRHD and normal individuals, which persisted up to 48 weeks. The percentage of CD25 + cells in both types of PBMC cultures directly correlated with the percentage of CD4 + cells and not with CD8 + cells in active rheumatic patients only. These findings indicate that the immune response in ARF and ARHD patients is skewed to produce activated helper T cells that release IL‐2 which drives the accumulation of more T helper cells. The result is an undamped helper T cell response in the peripheral blood of these patients.