期刊
NATURE IMMUNOLOGY
卷 8, 期 1, 页码 84-91出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1416
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- NCI NIH HHS [R01-CA87076] Funding Source: Medline
- NIAID NIH HHS [R01-AI42532, T32-AI07495, R01-AI066895] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA087076] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI042532, T32AI007495, R01AI066895] Funding Source: NIH RePORTER
HPK1 is a Ste20-related serine-threonine kinase that inducibly associates with the adaptors SLP-76 and Gads after T cell receptor ( TCR) signaling. Here, HPK1 deficiency resulted in enhanced TCR-induced phosphorylation of SLP-76, phospholipase C-gamma 1 and the kinase Erk, more-persistent calcium flux, and increased production of cytokines and antigen-specific antibodies. Furthermore, HPK1-deficient mice were more susceptible to experimental autoimmune encephalomyelitis. Although the interaction between SLP-76 and Gads was unaffected, the inducible association of SLP-76 with 14-3-3 tau ( a phosphorylated serine-binding protein and negative regulator of TCR signaling) was reduced in HPK1-deficient T cells after TCR stimulation. HPK1 phosphorylated SLP-76 and induced the interaction of SLP-76 with 14-3-3 tau. Our results indicate that HPK1 negatively regulates TCR signaling and T cell-mediated immune responses.
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