SEROLOGICAL ABNORMALITIES INDUCED BY ENGRAFTMENT OF VIABLE MOTH-EATENHEMATOPOIETIC-CELLS IN NUDE BEIGE RECIPIENTS

C57BL/6J (B6) mice homozygous for the viable motheaten (me(v)) mutatio n are short-lived and display severe immunodeficiency, autoimmunity an d inflammatory disease. B6 mice doubly homozygous for the nude (nu) an d beige (bg) mutations (nubg mice) are also short-lived and immunodefi cient. Nevertheless, grafts of me(v) lympho-hematopoietic cells increa sed life expectancy of nubg recipients. Such [me(v) --> nubg] chimeras did not develop any me(v)-like inflammatory pathology but showed auto immunity features, particularly hyperglobulinemia which, unlike the me (v) one, was due to IgG rather than IgM. Serological studies of [me(v) Igh(b) --> nubg Igh(a)] chimeras suprisingly revealed the exclusive h ost B-cell origin of the IgG2a overproduced by these chimeras. Yet, ab out half of such chimera serum IgM being IgM(b), me(v) B cells had act ually engrafted the nubg hosts. Together with the lack of transfer of the inflammatory pathology, this suggests that a non-me(v) environment might succeed acting as a regulator of some me(v)-induced dysfunction s.