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.