MHC class I cross-talk with CD2 and CD28 induces specific intracellular signalling and leads to growth retardation and apoptosis via a p56(lck)-dependent mechanism.

M Ruhwald; Anders Elm Pedersen; M H Claesson

MHC class I cross-talk with CD2 and CD28 induces specific intracellular signalling and leads to growth retardation and apoptosis via a p56(lck)-dependent mechanism.

M Ruhwald, Anders Elm Pedersen, M H Claesson

Department of Immunology and Microbiology

8 Citations (Scopus)

Abstract

Ligation of the major histocompatibility complex class I molecules (MHC-I) on human T lymphoma cells (Jurkat) initiates p56(lck)-dependent intracellular signalling events (phosphotyrosine kinase activity; [Ca(2+)](i)) and leads to augmented growth inhibition and apoptosis. MHC-I ligation in concert with ligation of CD2 or CD28 augments, changes or modifies the pattern of activation. Ligation of MHC-I and CD2 alone resulted in growth inhibition, whereas CD28 ligation alone had no effect on cell proliferation. Ligation of MHC-I together with CD2 augmented growth inhibition and enhanced the level of apoptosis. In parallel experiments with the p56(lck)-negative Jurkat mutant cell, JCaM1.6, cross-linking neither influenced cell signalling nor cellular growth functions, indicating a cardinal role of the src kinases in signal transduction via MHC-I, CD2 and CD28 molecules. The results presented here provide evidence for the involvement of MHC-I molecules in the modulation of signal transduction via the CD2 and CD28 costimulatory molecules. Copyright Copyright 1999 S. Karger AG, Basel

Original language	English
Journal	Experimental and Clinical Immunogenetics
Volume	16
Issue number	4
Pages (from-to)	199-211
Number of pages	12
ISSN	0254-9670
Publication status	Published - 1999

Cite this

MHC class I cross-talk with CD2 and CD28 induces specific intracellular signalling and leads to growth retardation and apoptosis via a p56(lck)-dependent mechanism. / Ruhwald, M; Pedersen, Anders Elm ; Claesson, M H.

In: Experimental and Clinical Immunogenetics, Vol. 16, No. 4, 1999, p. 199-211.

Research output: Contribution to journal › Journal article › Research › peer-review

@article{ee9ec760ac0511ddb5e9000ea68e967b,

title = "MHC class I cross-talk with CD2 and CD28 induces specific intracellular signalling and leads to growth retardation and apoptosis via a p56(lck)-dependent mechanism.",

abstract = "Ligation of the major histocompatibility complex class I molecules (MHC-I) on human T lymphoma cells (Jurkat) initiates p56(lck)-dependent intracellular signalling events (phosphotyrosine kinase activity; [Ca(2+)](i)) and leads to augmented growth inhibition and apoptosis. MHC-I ligation in concert with ligation of CD2 or CD28 augments, changes or modifies the pattern of activation. Ligation of MHC-I and CD2 alone resulted in growth inhibition, whereas CD28 ligation alone had no effect on cell proliferation. Ligation of MHC-I together with CD2 augmented growth inhibition and enhanced the level of apoptosis. In parallel experiments with the p56(lck)-negative Jurkat mutant cell, JCaM1.6, cross-linking neither influenced cell signalling nor cellular growth functions, indicating a cardinal role of the src kinases in signal transduction via MHC-I, CD2 and CD28 molecules. The results presented here provide evidence for the involvement of MHC-I molecules in the modulation of signal transduction via the CD2 and CD28 costimulatory molecules. Copyright Copyright 1999 S. Karger AG, Basel",

author = "M Ruhwald and Pedersen, {Anders Elm} and Claesson, {M H}",

note = "Keywords: Antigens, CD; Antigens, CD2; Antigens, CD28; Antigens, Differentiation, T-Lymphocyte; Apoptosis; Calcium; Cell Division; Flow Cytometry; Histocompatibility Antigens Class I; Humans; Jurkat Cells; Lymphocyte Specific Protein Tyrosine Kinase p56(lck); Phosphotyrosine; Protein-Tyrosine Kinases; Receptor Cross-Talk; Signal Transduction",

year = "1999",

language = "English",

volume = "16",

pages = "199--211",

journal = "Experimental and Clinical Immunogenetics",

issn = "0254-9670",

publisher = "S Karger AG",

number = "4",

}

TY - JOUR

T1 - MHC class I cross-talk with CD2 and CD28 induces specific intracellular signalling and leads to growth retardation and apoptosis via a p56(lck)-dependent mechanism.

AU - Ruhwald, M

AU - Pedersen, Anders Elm

AU - Claesson, M H

N1 - Keywords: Antigens, CD; Antigens, CD2; Antigens, CD28; Antigens, Differentiation, T-Lymphocyte; Apoptosis; Calcium; Cell Division; Flow Cytometry; Histocompatibility Antigens Class I; Humans; Jurkat Cells; Lymphocyte Specific Protein Tyrosine Kinase p56(lck); Phosphotyrosine; Protein-Tyrosine Kinases; Receptor Cross-Talk; Signal Transduction

PY - 1999

Y1 - 1999

N2 - Ligation of the major histocompatibility complex class I molecules (MHC-I) on human T lymphoma cells (Jurkat) initiates p56(lck)-dependent intracellular signalling events (phosphotyrosine kinase activity; [Ca(2+)](i)) and leads to augmented growth inhibition and apoptosis. MHC-I ligation in concert with ligation of CD2 or CD28 augments, changes or modifies the pattern of activation. Ligation of MHC-I and CD2 alone resulted in growth inhibition, whereas CD28 ligation alone had no effect on cell proliferation. Ligation of MHC-I together with CD2 augmented growth inhibition and enhanced the level of apoptosis. In parallel experiments with the p56(lck)-negative Jurkat mutant cell, JCaM1.6, cross-linking neither influenced cell signalling nor cellular growth functions, indicating a cardinal role of the src kinases in signal transduction via MHC-I, CD2 and CD28 molecules. The results presented here provide evidence for the involvement of MHC-I molecules in the modulation of signal transduction via the CD2 and CD28 costimulatory molecules. Copyright Copyright 1999 S. Karger AG, Basel

AB - Ligation of the major histocompatibility complex class I molecules (MHC-I) on human T lymphoma cells (Jurkat) initiates p56(lck)-dependent intracellular signalling events (phosphotyrosine kinase activity; [Ca(2+)](i)) and leads to augmented growth inhibition and apoptosis. MHC-I ligation in concert with ligation of CD2 or CD28 augments, changes or modifies the pattern of activation. Ligation of MHC-I and CD2 alone resulted in growth inhibition, whereas CD28 ligation alone had no effect on cell proliferation. Ligation of MHC-I together with CD2 augmented growth inhibition and enhanced the level of apoptosis. In parallel experiments with the p56(lck)-negative Jurkat mutant cell, JCaM1.6, cross-linking neither influenced cell signalling nor cellular growth functions, indicating a cardinal role of the src kinases in signal transduction via MHC-I, CD2 and CD28 molecules. The results presented here provide evidence for the involvement of MHC-I molecules in the modulation of signal transduction via the CD2 and CD28 costimulatory molecules. Copyright Copyright 1999 S. Karger AG, Basel

M3 - Journal article

C2 - 10575274

SN - 0254-9670

VL - 16

SP - 199

EP - 211

JO - Experimental and Clinical Immunogenetics

JF - Experimental and Clinical Immunogenetics

IS - 4

ER -

MHC class I cross-talk with CD2 and CD28 induces specific intracellular signalling and leads to growth retardation and apoptosis via a p56(lck)-dependent mechanism.

Abstract

Fingerprint

Cite this