Journal
SCIENTIFIC REPORTS
Volume 5, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep07688
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Funding
- NIH grant [AI051626, AI073955]
- USDA-NIFA postdoctoral fellowship
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Vaccine efficacy depends on strong long-term development of immune memory and the formation of memory CD8(+) T cells is critical for recall responses to infection. Upon antigen recognition by naive T cells, the strength of the TcR signal influences the subsequent effector and memory cells differentiation. Here, we have examined the role of Itk, a tyrosine kinase critical for TcR signaling, in CD8(+) effector and memory T cell differentiation during Listeria monocytogenes infection. We found that the reduced TcR signal strength in Itk deficient naive CD8(+) T cells enhances the generation of memory T cells during infection. This is accompanied by increased early Eomesodermin, IL-7R alpha expression and memory precursor effector cells. Furthermore, Itk is required for optimal cytokine production in responding primary effector cells, but not secondary memory responses. Our data suggests that Itk-mediated signals control the expression of Eomesodermin and IL-7R alpha, thus regulating the development of memory CD8(+) T cells, but not subsequent response of memory cells.
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