Probing immune functions in RAG-deficient mice

Curr Opin Immunol. 1994 Apr;6(2):313-9. doi: 10.1016/0952-7915(94)90107-4.


Inactivation of recombination activating gene (RAG)-1 or RAG-2 in mice results in the inability of developing lymphocytes to initiate V(D)J recombination, leading to the arrest of lymphocyte differentiation at a very early stage. Introduction of functionally assembled antigen-receptor genes or other potentially relevant genes into the RAG-deficient background can bypass the V(D)J recombination block and promote differentiation of the lymphocytes of RAG-deficient mice to various stages. This approach offers new means for analyzing the control of lymphocyte differentiation. In addition, generation of somatic chimeric mice by injecting mutant embryonic stem cells into the RAG-2-deficient blastocysts has also provided a powerful new method for assaying the potential roles of genes or regulatory elements in lymphocyte development or function.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • B-Lymphocytes / physiology
  • Cell Differentiation / genetics
  • DNA-Binding Proteins*
  • Genes, RAG-1*
  • Immune System / growth & development
  • Immune System / physiology*
  • Mice
  • Proteins / genetics*
  • Recombination, Genetic / genetics
  • T-Lymphocytes / physiology


  • DNA-Binding Proteins
  • Proteins
  • Rag2 protein, mouse
  • V(D)J recombination activating protein 2