Partial impairment of cytokine responses in Tyk2-deficient mice

被引：344

作者：

Karaghiosoff, M

Neubauer, H

Lassnig, C

Kovarik, P

Schindler, H

Pircher, H

McCoy, B

Bogdan, C

Decker, T

Brem, G

Pfeffer, K

Müller, M

机构：

[1] Vet Univ Vienna, Inst Genet & Anim Breeding, A-1210 Vienna, Austria

[2] Tech Univ Munich, Inst Med Microbiol Immunol & Hyg, D-81675 Munich, Germany

[3] IFA Tulln, Dept Biotechnol Anim Prod, A-3430 Tulln, Austria

[4] Vienna Bioctr, Inst Microbiol & Genet, A-1030 Vienna, Austria

[5] Univ Erlangen Nurnberg, Inst Clin Microbiol Immunol & Hyg, D-91054 Erlangen, Germany

[6] Univ Freiburg, Dept Immunol, Inst Med Microbiol & Hyg, D-79104 Freiburg, Germany

[7] Ludwig Boltzman Inst Immuno Cyto & Mol Genet, A-1210 Vienna, Austria

来源：

IMMUNITY | 2000年 / 13卷 / 04期

基金：

奥地利科学基金会;

关键词：

D O I：

10.1016/S1074-7613(00)00054-6

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

To assess the role of the Janus kinase (Jak) family member Tyk2, we have generated Tyk2(-/-) mice. In contrast to other Jaks, where inactivation leads to a complete loss of the respective cytokine receptor signal, Tyk2(-/-) mice display reduced responses to IFN alpha/beta and IL-12 and a selective deficiency in Stat3 activation in these pathways. Unexpectedly, lFN gamma signaling is also impaired in Tyk2(-/-) mice. Tyk2(-/-) macrophages fail to produce nitric oxide upon lipopolysaccharide induction. Tyk2(-/-) mice are unable to clear vaccinia virus and show a reduced T cell response after LCMV challenge. These data imply a selective contribution of Tyk2 to the signals triggered by various biological stimuli and cytokine receptors.

引用

页码：549 / 560

页数：12

共 64 条

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