Imbalance towards Th1 predominance is associated with acceleration of lupus-like autoimmune syndrome in MRL mice.

Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.

Imbalance towards Th1 predominance is associated with acceleration of lupus-like autoimmune syndrome in MRL mice.

J Clin Invest. 1996 Apr 1;97(7):1597-604. Unique Identifier : AIDSLINE MED/96181558
Takahashi S; Fossati L; Iwamoto M; Merino R; Motta R; Kobayakawa T; Izui S; Department of Pathology, Centre Medical Universitaire,; University of Geneva, Switzerland.

Abstract: To investigate the respective roles of Th1 and Th2 cells in the pathogenesis of lupus-like autoimmune disease, we have analyzed the spontaneous and antigen-induced productions of IgG1 vs IgG2a and IgG3 subclasses in relation to the mRNA expression of INF-gamma (Th1 cytokine promoting IgG2a and IgG3 production), IL-4 (Th2 cytokine promoting IgG1 production), and IL-10 (Th2 cytokine) in CD4+ T cells from lupus-prone MRL mice. For this purpose, two paired sets of MRL mice were chosen for the comparison of these parameters: (a) MRL-lpr/lpr (lpr for lymphoproliferation) and its recently described substrain with a prolonged survival, termed MRL-lpr/lpr.ll (ll for long lived) and (b) MRL male mice bearing the Yaa (Y-linked autoimmune acceleration) gene (MRL.Yaa) with an accelerated disease and their male counterparts lacking the Yaa gene. We demonstrate herein that the accelerated development of lupus-like autoimmune disease in MRL-lpr/lpr and MRL.Yaa mice, as compared with MRL-lpr/lpr.ll and MRL-+/+ mice, respectively, was correlated with an enhanced expression of IFN-gamma vs IL-4 and IL-10 mRNA in CD4+ T cells, which paralleled with an increase of spontaneous and foreign T cell-dependent antigen-induced productions of IgG2a and IgG3 vs IgG1 antibodies. These data suggest that an imbalance towards Th1 predominance may play a significant role in the acceleration of lupus-like autoimmune disease in MRL mice.

Keywords: Animal Antigens/ADMINISTRATION & DOSAGE Autoimmune Diseases/ETIOLOGY/GENETICS/*IMMUNOLOGY Base Sequence DNA Primers/GENETICS Female Gene Expression Human IgG/BIOSYNTHESIS/BLOOD/CLASSIFICATION Interferon Type II/GENETICS Interleukin-10/GENETICS Interleukin-4/GENETICS Lupus Erythematosus, Systemic/ETIOLOGY/GENETICS/*IMMUNOLOGY Male Mice Mice, Mutant Strains Molecular Sequence Data RNA, Messenger/GENETICS/METABOLISM Support, Non-U.S. Gov't Th1 Cells/*IMMUNOLOGY Th2 Cells/IMMUNOLOGY JOURNAL ARTICLE
960730
M9670452

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