BALB/c.CBA/N mice carrying the defective Btk(xid) gene are resistant to pristane-induced plasmacytomagenesis

The X-chromosome from the CBA/N mouse which carries the defective Bruton's tyrosine kinase (Btk) allele (X-xid) has been introgressively backcrossed o nto the plasmacytoma (PCT) induction-susceptible BALB/cAN. Inbred BALB/c.CB A/N-xid/xid (C.CBA/N) mice raised and maintained in our conventional colony were given three 0.5 mi injections of pristane and were highly refractory to PCT induction. Only one PCT was found among 59 mice followed for greater than or equal to 300 days. Twenty mice were examined at day 200 for foci o f plasma cells in the oil granuloma. Ten mice had small foci of plasma cell s, most of which were plasmacytotic, embedded in the inflammatory oil granu loma. In one there were multiple foci, but most of the mice had only one or two foci. F-1 hybrid (XY)-Y-xid males derived from CBA/N females crossed t o BALB/cAnPt were also resistant to PCT induction, while heterozygous and h omozygous XY males were susceptible. C.CBA/N mice can develop extensive muc osal plasma cells as well as plasma cell accumulations in oil granuloma tis sue, but the precursors of these plasma cells do not give rise to PCT in ge netically susceptible hosts. The failure of C.CBA/N mice to develop PCT is probably due to the elimination of B cell clones that can be perpetuated by repeated exposure to thymus-independent type 2 antigens.