A LAT mutation that inhibits T cell development yet induces lymphoproliferation

Science. 2002 Jun 14;296(5575):2040-3. doi: 10.1126/science.1069066.

Abstract

Mice homozygous for a single tyrosine mutation in LAT (linker for activation of T cells) exhibited an early block in T cell maturation but later developed a polyclonal lymphoproliferative disorder and signs of autoimmune disease. T cell antigen receptor (TCR)-induced activation of phospholipase C-gamma1 (PLC-gamma1) and of nuclear factor of activated T cells, calcium influx, interleukin-2 production, and cell death were reduced or abrogated in T cells from LAT mutant mice. In contrast, TCR-induced Erk activation was intact. These results identify a critical role for integrated PLC-gamma1 and Ras-Erk signaling through LAT in T cell development and homeostasis.

MeSH terms

  • Adaptor Proteins, Signal Transducing*
  • Animals
  • Antibodies, Antinuclear / blood
  • Autoimmune Diseases / immunology
  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / physiology
  • CD5 Antigens / analysis
  • Calcium / metabolism
  • Calcium Signaling
  • Carrier Proteins / genetics*
  • Carrier Proteins / physiology*
  • Cell Division
  • Interleukin-2 / biosynthesis
  • Isoenzymes / metabolism*
  • Lymphocyte Activation
  • Lymphoproliferative Disorders / etiology*
  • Lymphoproliferative Disorders / immunology
  • Lymphoproliferative Disorders / pathology
  • MAP Kinase Signaling System
  • Membrane Proteins*
  • Mice
  • Mice, Inbred C57BL
  • Mitogen-Activated Protein Kinases / metabolism
  • Phenotype
  • Phospholipase C gamma
  • Phosphoproteins / genetics*
  • Phosphoproteins / physiology*
  • Phosphorylation
  • Point Mutation*
  • Receptors, Antigen, T-Cell / immunology
  • Receptors, Antigen, T-Cell / metabolism
  • Signal Transduction
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / physiology
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / physiology
  • Thymus Gland / cytology
  • Thymus Gland / immunology
  • Thymus Gland / pathology
  • Transcription Factors / metabolism
  • Type C Phospholipases / metabolism*
  • ras Proteins / metabolism

Substances

  • Adaptor Proteins, Signal Transducing
  • Antibodies, Antinuclear
  • CD5 Antigens
  • Carrier Proteins
  • Interleukin-2
  • Isoenzymes
  • Lat protein, mouse
  • Membrane Proteins
  • Phosphoproteins
  • Receptors, Antigen, T-Cell
  • Transcription Factors
  • Mitogen-Activated Protein Kinases
  • Type C Phospholipases
  • Phospholipase C gamma
  • ras Proteins
  • Calcium