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Notch signaling regulates antigen sensitivity of naive CD4+ T cells by tuning co-stimulation.

Abstract：

:Adaptive immune responses begin when naive CD4(+) T cells engage peptide+major histocompatibility complex class II and co-stimulatory molecules on antigen-presenting cells (APCs). Notch signaling can influence effector functions in differentiated CD4(+) T helper and T regulatory cells. Whether and how ligand-induced Notch signaling influences the initial priming of CD4(+) T cells has not been addressed. We have found that Delta Like Ligand 4 (DLL4)-induced Notch signaling potentiates phosphatidylinositol 3-OH kinase (PI3K)-dependent signaling downstream of the T cell receptor+CD28, allowing naive CD4(+) T cells to respond to lower doses of antigen. In vitro, DLL4-deficient APCs were less efficient stimulators of CD4(+) T cell activation, metabolism, proliferation, and cytokine secretion. With deletion of DLL4 from CD11c(+) APCs in vivo, these deficits translated to an impaired ability to mount an effective CD4(+)-dependent anti-tumor response. These data implicate Notch signaling as an important regulator of adaptive immune responses.

journal_name

Immunity

journal_title

Immunity

authors

Laky K,Evans S,Perez-Diez A,Fowlkes BJ

doi

10.1016/j.immuni.2014.12.027

subject

Has Abstract

pub_date

2015-01-20 00:00:00

pages

80-94

issue

1

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(14)00494-4

journal_volume

42

pub_type

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