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Anti‐Interleukin‐2 Receptor Monoclonal Antibody Therapy Supports a Role for Thl‐Like Cells in HgCl 2 ‐Induced Autoimmunity in Rats
Author(s) -
DUBEY D.,
KUHN J.,
VIAL M. C.,
DRUET P.,
BELLON B.
Publication year - 1993
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.1365-3083.1993.tb03311.x
Subject(s) - monoclonal antibody , polyclonal antibodies , autoimmunity , immune system , immunology , antibody , chemistry , autoimmune disease , microbiology and biotechnology , endocrinology , biology
Brown‐Norway (BN) rats injected with HgCl 2 develop an autoimmune disease characterized by a T dependent polyclonal B‐cell activation. Increase in major histocompatibility complex class II molecule expression on B cells concomitant with enhancement of serum IgE concentration supports the involvement of the T helper 2 (Th2)‐like subset in the induction of the disease. The mercury disease is autoreguiated and does not develop in Lewis (LEW) rats. Considering the reciprocal regulation, well defined in mice, between the Th1 and Th2 subsets, we addressed the role of the Thl‐like subset in this disease. Brown‐Norway and LEW rats injected with HgCl 2 were treated wilh NDS61, a mouse anti‐ral‐IL‐2R MoAb that blocks mainly Th1 cells. Data reported herein show that: (1) HgCl 2 treatment does not modify either the percentage of IL‐2R + cells or IL‐2R expression in both BN and LEW rats; (2) treatment of BN rats with NDS61 MoAb does not modify the induction phase of the mercury disease but delays in parl the regulation phase; (3) such a treatment leads lo some immune abnormalities in LEW rals; (4) HgCl 2 markedly potentiates the anti‐mouse Ig antibody response in BN rats which probably limits the effect of this treatment. This study supports a role for the Th1‐like subset in HgCl 2 ‐induced auloimmunity in the rat.