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Review
. 2020 Feb 28;48(1):179-185.
doi: 10.1042/BST20190486.

Tuning T helper cell differentiation by ITK

Affiliations
Review

Tuning T helper cell differentiation by ITK

Jessica P Elmore et al. Biochem Soc Trans. .

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.

Keywords: Itk; T-cells; cytokines; kinase; signaling.

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Conflict of interest statement

Conflict of Interest disclosure

A.A. receives research support from 3M Corporation. The other authors have no commercial or financial conflicts of interest.

Figures

Figure 1.
Figure 1.. TCR tuning of TH differentiation.
A) Different TH effector cell fates that can emerge from early T cell activation and differentiation, and the cytokines that they produce. Green arrows indicate enhanced differentiation in the absence of ITK. Gray arrows indicate reduced differentiation in the absence of ITK. B) Depiction of specific TCR signaling networks downstream of ITK that influence Tr1 cells, TH17 cells and Treg cells as reported [, , , , , –78]. Inhibition or absence of Itk (depicted by the red arrows) results in reduced Tr1 cells, TH17 cells and enhanced Treg cells. Furthermore, inhibition or absence of Itk during TH17 differentiation results in enhanced Treg cells. Cytokines depicted are those involved in the specific TH cell fate differentiation.

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