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.

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 -