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Interleukin‐4 Gene Expression in Mercury‐Induced Autoimmunity
Author(s) -
GILLESPIE K. M.,
QASIM F. J.,
TIBBATTS L. M.,
THIRU S.,
OLIVEIRA D. B. G.,
MATHIESON P. W.
Publication year - 1995
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.1365-3083.1995.tb03563.x
Subject(s) - autoimmunity , gene expression , immunology , gene , biology , genetics , immune system
Mercuric chloride (HgCl 2 ) induces autoitnmunity in Brown Norway (BN) rats, with necrotizing vasculitis in the gut. Circumstantial evidence implicates the T h 2 subset of CD4 + T lymphocytes, which produces IL‐4. We developed a quantitative polymerase chain reaction (PCR) technique to quantify IL‐4 gene expression. A phagemid containing rat IL‐4 cDNA was modified to act as the template for a synthetic RNA construct; a known amount of synthetic RNA was added to total RNA from spleen and caecum of BN rats at various times after HgCl 2 , followed by reverse transcriptase PCR. IL‐4 gene expression increased markedly in spleen and caecum after HgCl 2 . Splenic levels peaked by 10 days at approximately five‐times baseline, then returned towards normal as the autoimmune response was spontaneously regulated. Caecal IL‐4 expression peaked at 48 h, at which time we observed a previously unreported early phase of tissue injury, with necrotizing vasculitis qualitatively similar to that reported previously in the later phases of the model. These data support a key role for IL‐4 in this experimental model of autoimmunity. The quantitative PCR technique can be modified for analysis of other cytokines, allowing further investigation of the role of T ceil subsets in this model.