Production of 17.2.25 μ transgenic and endogenous immunoglobulin in X‐linked immune deficient mice

In M54 mice transgenic for a completely rearranged μ^a heavy chain there is a decrease in total B cells and the rearrangement of endogenous immunoglobulin genes is partially inhibited. Surprisingly, however, endogenous immunoglobulin gene rearrangement and significant heavy chain polypeptide production does occur. We tested the hypothesis that only CD5⁺ B cells produce endogenous immunoglobulin by taking advantage of the fact that X‐linked immune deficient (xid) mice normally are deficient in CD5⁺ B cells. We found that the frequency of CD5⁺ splenic B cells was similar in X^xidY transgenic and non‐transgenic F₁ males, and in X^xidX transgenic and non‐transgenic F₁ females. In both X^xidX and X^xidY transgenic F₁ mice some, but not all, splenic B cells are CD11b⁺. There was a striking deficit of splenic B cells expressing endogenous immunoglobulin in X^xidY transgenic mice, although this was not true for peritoneal cells. Thus, the introduction of the 17.2.25 μ transgene does not prevent the development of CD5⁻ B cells nor does it limit endogenous immunoglobulin gene arrangement and expression solely to CD5⁺ B cells. However, in mice capable of expressing B cell surface CD5 or CD11 this transgene can lead to expansion of the fraction of B cells positive for these molecules. We conclude that while the introduction of the 17.2.25 μ transgene alters the frequencies of B cell populations maturation is not limited to one subpopulation.