B-cell-tropic interleukins in murine systemic lupus erythematosus (SLE) 1

Immunol Rev. 1984 Apr;78:159-83. doi: 10.1111/j.1600-065x.1984.tb00481.x.


Functional in vitro studies of B cells from 3 murine strains which develop severe early onset SLE-like disease with marked polyclonal B cell hyperactivity lead to the following conclusions: 1.) B cell proliferation and differentiation in lupus mice remains dependent on accessory signals of either macrophage or T cell origin; 2.) B cells from BXSB, NZB/W and MRL/1 mice appear to require the same number and type of signals as normal B cells to undergo polyclonal or antigen-directed responses. B cells of BXSB and NZB/W, but not MRL/1, origin differ from normal B cells by their higher sensitivity (or degree of response) to the signals they receive; 3.) Proliferating T cells in enlarged nodes and spleens of older MRL/1 mice, in the absence of mitogens, secrete in vitro abnormally high levels of a factor (L-BCDF) inducing terminal differentiation of activated B cells to Ig secreting cells. Based on these findings, murine SLE can be divided into 2 main types which may, nevertheless, share some characteristics: Type 1 murine SLE, characterized by primary B cell hyperresponsiveness to activating signals and lymphokines promoting B cell growth and differentiation (NZ and BXSB strains); and, Type 2 murine SLE, characterized by T helper cell hyperactivity and overproduction by proliferating T cells of one or more B cell differentiation factors (MRL/1 strain). In both types of murine SLE, abnormal responses to accessory signals or overproduction of differentiation-inducing signals ultimately leads to polyclonal and auto-antigen specific B cell expansion, hypergammaglobulinemia and auto-antibody production, and Ig gene rearrangement (IgM to IgG switching), resulting in the production of pathogenic IgG type auto-antibodies and disease.

Publication types

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

MeSH terms

  • Animals
  • Antigens, Differentiation, B-Lymphocyte
  • Antigens, Surface / immunology*
  • B-Lymphocytes / immunology*
  • Cell Differentiation
  • Cell Division
  • Disease Models, Animal*
  • Female
  • Growth Substances / immunology*
  • Immunoglobulin G / immunology
  • Interleukin-4
  • Lupus Erythematosus, Systemic / genetics
  • Lupus Erythematosus, Systemic / immunology*
  • Lupus Erythematosus, Systemic / veterinary
  • Lymphocyte Activation
  • Lymphocyte Cooperation
  • Lymphokines / immunology*
  • Macrophages / immunology
  • Male
  • Mice
  • Mice, Inbred Strains / immunology
  • Rodent Diseases / genetics
  • Rodent Diseases / immunology


  • Antigens, Differentiation, B-Lymphocyte
  • Antigens, Surface
  • Growth Substances
  • Immunoglobulin G
  • Lymphokines
  • Interleukin-4