Tuning T helper cell differentiation by ITK

Authors

Jessica P. Elmore, Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853, U.S.A.
Michael C. McGee, Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, U.S.A.
Natalie F. Nidetz, Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, U.S.A.
Orchi Anannya, Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853, U.S.A.
Weishan Huang, Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853, U.S.A.
Avery August, Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853, U.S.A.

Document Type

Article

Publication Date

2-28-2020

Abstract

CD4+ effector T cells effectuate T cell immune responses, producing cytokines to orchestrate the nature and type of immune responses. The non-receptor tyrosine kinase IL-2 inducible T cell kinase (ITK), a mediator of T cell Receptor signaling, plays a critical role in tuning the development of these effector cells. In this review we discussed the role that signals downstream of ITK, including the Ras/MAPK pathway, play in differentially controlling the differentiation of TH17, Foxp3+ T regulatory (Treg) cells, and Type 1 regulatory T (Tr1) cells, supporting a model of ITK signals controlling a decision point in the effector T cell differentiation process.

Publication Source (Journal or Book title)

Biochemical Society transactions

First Page

179

Last Page

185

Recommended Citation

Elmore, J. P., McGee, M. C., Nidetz, N. F., Anannya, O., Huang, W., & August, A. (2020). Tuning T helper cell differentiation by ITK. Biochemical Society transactions, 48 (1), 179-185. https://doi.org/10.1042/BST20190486