TY - JOUR
T1 - Natural killer activating receptors trigger interferon γ secretion from T cells and natural killer cells
AU - Mandelboim, Ofer
AU - Kent, Sally
AU - Davis, Daniel M.
AU - Wilson, S. Brian
AU - Okazaki, Taku
AU - Jackson, Richard
AU - Hafler, David
AU - Strominger, Jack L.
PY - 1998/3/31
Y1 - 1998/3/31
N2 - Proliferation of human CD4+ αβ T cells expressing a natural killer cell activating receptor (NKAR) has been shown to be enhanced, particularly in response to low doses of antigen, if the target cells present appropriate human class I major histocompatibility complex (MHC) molecules. Here, we show that NKAR also enhance proliferation and killing of target cells by subsets of CD8+ αβ and CD8+ γδ T cells, as well as by NK cells. Strikingly, interferon γ secretion from all of these types of lymphocytes was markedly increased by interaction of the NKAR with their MHC class I ligands, independently of enhancement of proliferation. Thus, the recognition of class I MHC molecules by NKAR on both T cells and NK cells may provide a regulatory mechanism that affects immune responses through the secretion of interferon and possibly other cytokines. It represents a signal for cytokine secretion alternative and/or augmentative to that through the T cell receptor.
AB - Proliferation of human CD4+ αβ T cells expressing a natural killer cell activating receptor (NKAR) has been shown to be enhanced, particularly in response to low doses of antigen, if the target cells present appropriate human class I major histocompatibility complex (MHC) molecules. Here, we show that NKAR also enhance proliferation and killing of target cells by subsets of CD8+ αβ and CD8+ γδ T cells, as well as by NK cells. Strikingly, interferon γ secretion from all of these types of lymphocytes was markedly increased by interaction of the NKAR with their MHC class I ligands, independently of enhancement of proliferation. Thus, the recognition of class I MHC molecules by NKAR on both T cells and NK cells may provide a regulatory mechanism that affects immune responses through the secretion of interferon and possibly other cytokines. It represents a signal for cytokine secretion alternative and/or augmentative to that through the T cell receptor.
UR - http://www.scopus.com/inward/record.url?scp=0032584204&partnerID=8YFLogxK
U2 - 10.1073/pnas.95.7.3798
DO - 10.1073/pnas.95.7.3798
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C2 - 9520447
AN - SCOPUS:0032584204
SN - 0027-8424
VL - 95
SP - 3798
EP - 3803
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 7
ER -
