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Absence of the T‐bet Gene Coding for the Th1‐Related Transcription Factor Does Not Affect Diabetes‐Associated Phenotypes in Balb/c Mice
Author(s) -
MELANITOU EVIE,
LIU EDWIN,
MIAO DONGMEI,
YU LIPING,
GLIMCHER LAURIE H.,
EISENBARTH GEORGE
Publication year - 2003
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1288.024
Subject(s) - insulitis , immune system , phenotype , biology , transcription factor , gene , immunology , autoimmunity , genetics
A bstract : The T‐box expressed in T cells gene (T‐bet) is a member of the T‐box family of transcription factors. T‐bet‐deficient mice show normal lymphoid development, but exhibit profound defects in their Th1‐mediated immune responses. As the balance between Th1‐ and Th2‐mediated immune responses plays a role in autoimmune‐prone diseases, we have investigated the diabetes‐related insulin autoantibody (IAA) and cellular immune responses (insulitis), in the absence of Th1 lineage commitment, in T‐bet KO Balb/c mice, after immunization with the B9‐23 insulin peptide. We have therefore investigated whether absence of the T‐bet gene influences diabetes‐related phenotypes in Balb/c T‐bet KO mice.