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IL‐12‐Deficient Mice Are Defective but Not Devoid of Type 1 Cytokine Responses
Author(s) -
MAGRAM JEANNE,
SFARRA JESSICA,
CONNAUGHTON SUZANNE,
FAHERTY DENISE,
WARRIER RAJEEV,
CARVAJAL DAISY,
WU CHANGYOU,
STEWART COLIN,
SARMIENTO ULLA,
GATELY MAURICE K.
Publication year - 1996
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 - 10.1111/j.1749-6632.1996.tb52655.x
Subject(s) - immune system , immunology , cytokine , biology , in vivo , phenotype , knockout mouse , immunity , interleukin 4 , humoral immunity , interleukin 12 , cellular immunity , microbiology and biotechnology , in vitro , cytotoxic t cell , gene , genetics
Interleukin-12 (IL-12) has been described as a pivotal molecule in the immune response based in part on its ability to influence the differentiation of T helper (Th) cells into a type 1 (Th1) phenotype. This event is crucial in that appropriate differentiation of naive T cells can determine susceptibility or resistance to given pathogens by influencing the balance between cellular and humoral immunity. In order to further delineate the role of IL-12 in the immune response, we generated mice deficient for this cytokine. IL-12 knockout mice were viable, fully fertile, and displayed no obvious developmental abnormalities. Upon immunological analysis, these mice demonstrated an impaired ability to effect a Th1 response as well as an impaired ability to produce interferon-gamma in response to endotoxin in vivo. These data establish an essential role for IL-12 in the generation of optimal Th1 responses in vivo, but weak responses can occur independently of IL-12.