The essential role of LAT in thymocyte development during transition from the double-positive to single-positive stage

J Immunol. 2009 May 1;182(9):5596-604. doi: 10.4049/jimmunol.0803170.

Abstract

The linker for activation of T cells (LAT) is an adaptor protein that couples TCR engagement to downstream signaling cascades. LAT is important in early thymocyte development as LAT-deficient mice have a complete block at the double-negative (DN) 3 stage. To study the role of LAT beyond the DN3 stage, we generated mice in which the lat gene could be deleted by the Cre recombinase. Analysis of these mice showed that deletion of LAT after the DN3 stage allowed thymocytes to develop past the DN3 to DN4 checkpoint and to generate double-positive thymocytes. However, LAT-deficient DP thymocytes were severely defective in responding to stimulation via the TCR and failed to differentiate into single-positive thymocytes efficiently. Consequently, few LAT-deficient mature T cells could be found in the periphery. These T cells had undergone extensive homeostatic proliferation and expressed low levels of the TCR on their surface. Collectively, our data indicate that in addition to its role in pre-TCR signaling, LAT also plays an essential role in thymocyte development during transition from the double-positive to single-positive stage.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / deficiency
  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / physiology*
  • Animals
  • CD4 Antigens / biosynthesis*
  • CD4 Antigens / genetics
  • CD8 Antigens / biosynthesis*
  • CD8 Antigens / genetics
  • Cell Differentiation / genetics
  • Cell Differentiation / immunology*
  • Gene Deletion
  • Gene Knock-In Techniques
  • Membrane Proteins / deficiency
  • Membrane Proteins / genetics
  • Membrane Proteins / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Mutant Strains
  • Mice, Transgenic
  • Phosphoproteins / deficiency
  • Phosphoproteins / genetics
  • Phosphoproteins / physiology*
  • Receptors, Antigen, T-Cell / physiology
  • Signal Transduction / genetics
  • Signal Transduction / immunology
  • Thymus Gland / cytology*
  • Thymus Gland / immunology*
  • Thymus Gland / metabolism

Substances

  • Adaptor Proteins, Signal Transducing
  • CD4 Antigens
  • CD8 Antigens
  • Lat protein, mouse
  • Membrane Proteins
  • Phosphoproteins
  • Receptors, Antigen, T-Cell