Abrogation of murine lupus by the xid gene is associated with reduced responsiveness of B cells to T-cell-helper signals.
Introduction of the xid genetic mutation into strains of mice (NZB, MRL/1, BXSB), which are normally susceptible to a lupus-like disorder, significantly delays the onset of disease and reduces the polyclonal B-cell activation characteristic of the lupus-prone strains. Evidence is presented here which shows that B cells from NZB and MRL/1 mice which carry the xid mutation have drastically reduced responses to T-cell-derived B-cell-growth- and differentiation-inducing activities. These results are in accord with a theory that acceleration of lupus onset may be due to overproduction of and/or increased responsiveness to B-cell activation signals.
D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D002454:Cell Differentiation; D006133:Growth Substances / Q000276:immunology; D015847:Interleukin-4; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D008211:Lymphocyte Cooperation; D008222:Lymphokines / Q000276:immunology; D051379:Mice; D008814:Mice, Inbred NZB / Q000276:immunology; D008817:Mice, Mutant Strains / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology
D006133:Growth Substances; D008222:Lymphokines; D015847:Interleukin-4