Signal transduction through Vav-2 participates in humoral immune responses and B cell maturation

Nat Immunol. 2001 Jun;2(6):542-7. doi: 10.1038/88748.

Abstract

B and T lymphocytes develop normally in mice lacking the guanine nucleotide exchange factor Vav-2. However, the immune responses to type II thymus-independent antigen as well as the primary response to thymus-dependent (TD) antigen are defective. Vav-2-deficient mice are also defective in their ability to switch immunoglobulin class, form germinal centers and generate secondary immune responses to TD antigens. Mice lacking both Vav-1 and Vav-2 contain reduced numbers of B lymphocytes and display a maturational block in the development of mature B cells. B cells from Vav-1(-/-)Vav-2(-/-) mice respond poorly to antigen receptor triggering, both in terms of proliferation and calcium release. These studies show the importance of Vav-2 in humoral immune responses and B cell maturation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibody Formation*
  • Antigens, Differentiation, T-Lymphocyte / immunology
  • Antigens, T-Independent / immunology
  • B-Lymphocytes / cytology*
  • B-Lymphocytes / immunology*
  • Cell Cycle Proteins*
  • Cell Differentiation
  • Mice
  • Mice, Knockout
  • Oncogene Proteins / genetics
  • Oncogene Proteins / immunology*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / immunology
  • Proto-Oncogene Proteins c-vav
  • Signal Transduction

Substances

  • Antigens, Differentiation, T-Lymphocyte
  • Antigens, T-Independent
  • Cell Cycle Proteins
  • Oncogene Proteins
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-vav
  • Vav1 protein, mouse
  • Vav2 protein, mouse