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Induced expression of Fc?RIIIa (CD16a) on CD4+ T cells triggers generation of IFN-?high subset.


ABSTRACT: Whether or not CD4(+) T-cells express low affinity receptor Fc?RIIIa (CD16a) in disease pathology has not been examined in great detail. In this study, we show that a subset of activated CD4(+) T-cells in humans express Fc?RIIIa. The ligation of Fc?RIIIa by immune complexes (ICs) in human CD4(+) T-cells produced co-stimulatory signal like CD28 that triggered IFN-? production. The induced expression of Fc?RIIIa on CD4(+) helper T-cells is an important finding since these receptors via ITAM contribute to intracellular signaling. The induced expression of Fc?RIIIa on CD4(+) T helper cells and their ability to co-stimulate T-cell activation are important and novel findings that may reveal new pathways to regulate adaptive immune responses during inflammation and in autoimmunity.

SUBMITTER: Chauhan AK 

PROVIDER: S-EPMC4335247 | biostudies-literature | 2015 Feb

REPOSITORIES: biostudies-literature

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Induced expression of FcγRIIIa (CD16a) on CD4+ T cells triggers generation of IFN-γhigh subset.

Chauhan Anil K AK   Chen Chen C   Moore Terry L TL   DiPaolo Richard J RJ  

The Journal of biological chemistry 20150102 8


Whether or not CD4(+) T-cells express low affinity receptor FcγRIIIa (CD16a) in disease pathology has not been examined in great detail. In this study, we show that a subset of activated CD4(+) T-cells in humans express FcγRIIIa. The ligation of FcγRIIIa by immune complexes (ICs) in human CD4(+) T-cells produced co-stimulatory signal like CD28 that triggered IFN-γ production. The induced expression of FcγRIIIa on CD4(+) helper T-cells is an important finding since these receptors via ITAM contri  ...[more]

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