期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 195, 期 7, 页码 801-810出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20011481
关键词
viral infection; cellular activation; T lymphocytes; protein kinases; lymphocytic choriomeningitis virus
资金
- Canadian Institutes of Health Research [37368-1] Funding Source: Medline
- NIAID NIH HHS [AI09484, R01 AI009484] Funding Source: Medline
c-Jun NH2-terminal kinases (JNK) play important roles in T helper cell (Th) proliferation, differentiation, and maintenance of Th1/Th2 polarization. To determine whether JNKs are involved in antiviral T cell immunity and whether JNK1 and JNK2 bear biological differences, we investigated the immune responses of JNK1-deficient and JNK2-deficient mice to lymphocytic choriomeningitis virus (LCMV). After LCMV infection, wild-type (JNK1(+/+)) m-ice had a 5- to 10-fold increase in splenic CD8(+) T cells. In contrast, infected JNK1(-/-) mice showed a significantly lower virus-specific CD8(+) T cell expansion. However, JNK1(-/-) mice cleared LCMV infection with similar kinetics as JNK mice. Splenic T cells from LCMV-infected JNK I animals produced interferon gamma after stimulation with viral peptides. However, fewer JNK1(-/-) T cells acquired an activated phenotype (CD44(hi)) and more JNK1(-/-)CD8(+)CD44(hi) cells underwent apoptosis than JNK(+/+) cells at the peak of the primary response. In contrast, LCMV-infected JNK2(-/-) mice generated more virus-specific CD8(+) T cells than JNK(+/+) mice. These results indicate that JNK1 and JNK2 signal pathways have distinct roles in T cell responses during a viral infection. JNK1 is involved in survival of activated T cells during immune responses, and JNK2 plays a role in control of CD8(+) T cell expansion in vivo.
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