How Lipid-Specific T Cells Become Effectors: The Differentiation of iNKT Subsets.

Haiguang Wang,Kristin A. Hogquist

doi:10.3389/fimmu.2018.01450

Haiguang Wang, Kristin A. Hogquist

Open Access

https://doi.org/10.3389/fimmu.2018.01450

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Abstract

In contrast to peptide-recognizing T cells, invariant natural killer T (iNKT) cells express a semi-invariant T cell receptor that specifically recognizes self- or foreign-lipids presented by CD1d molecules. There are three major functionally distinct effector states for iNKT cells. Owning to these innate-like effector states, iNKT cells have been implicated in early protective immunity against pathogens. Yet, growing evidence suggests that iNKT cells play a role in tissue homeostasis as well. In this review, we discuss current knowledge about the underlying mechanisms that regulate the effector states of iNKT subsets, with a highlight on the roles of a variety of transcription factors and describe how each subset influences different facets of thymus homeostasis.

Highlights

Natural killer T cells (NKT) were named because they express T cell receptor (TCR)–CD3 complexes as well as the natural killer (NK) cell receptor NK1.1 (CD161) [1, 2]
While playing a central role in invariant natural killer T (iNKT) cell development, PLZF is initially induced in the stage 0 iNKT cells, and its expression can be regulated by the transcription factor Runx1 through direct binding to a critical enhancer of PLZF gene [64]
Taken together, considering that maturation of iNKT cells after positive selection of stage 0 iNKT cells requires the presence of CD1d in the thymus [86], it is possible that the endogenous lipid ligands for iNKT cells are presented in both thymic cortex and medulla and are displayed by different antigenpresenting cells (APCs)

Summary

Introduction

Natural killer T cells (NKT) were named because they express T cell receptor (TCR)–CD3 complexes as well as the natural killer (NK) cell receptor NK1.1 (CD161) [1, 2]. Egr2 Strong TCR signaling in stage 0 iNKT cells commits their fate to iNKT lineage, as it leads to elevated expression of the transcription factors Egr1 and Egr2, which influence further development of iNKT cells [36].

Results

Conclusion