Costimulation of CD8alphabeta T cells by NKG2D via engagement by MIC induced on virus-infected cells.
Nat Immunol
; 2(3): 255-60, 2001 Mar.
Article
em En
| MEDLINE
| ID: mdl-11224526
ABSTRACT
NKG2D is an activating receptor that stimulates innate immune responses by natural killer cells upon engagement by MIC ligands, which are induced by cellular stress. Because NKG2D is also present on most CD8alphabeta T cells, it may modulate antigen-specific T cell responses, depending on whether MIC molecules--distant homologs of major histocompatibility complex (MHC) class I with no function in antigen presentation--are induced on the surface of pathogen-infected cells. We found that infection by cytomegalovirus (CMV) resulted in substantial increases in MIC on cultured fibroblast and endothelial cells and was associated with induced MIC expression in interstitial pneumonia. MIC engagement of NKG2D potently augmented T cell antigen receptor (TCR)-dependent cytolytic and cytokine responses by CMV-specific CD28- CD8alphabeta T cells. This function overcame viral interference with MHC class I antigen presentation. Combined triggering of TCR-CD3 complexes and NKG2D induced interleukin 2 production and T cell proliferation. Thus NKG2D functioned as a costimulatory receptor that can substitute for CD28.
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Base de dados:
MEDLINE
Assunto principal:
Ativação Linfocitária
/
Receptores Imunológicos
/
Antígenos de Histocompatibilidade Classe I
/
Receptores de Antígenos de Linfócitos T alfa-beta
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Linfócitos T CD8-Positivos
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Citomegalovirus
Idioma:
En
Ano de publicação:
2001
Tipo de documento:
Article