Serological Abnormalities Induced by Engraftment of Viable Motheaten Hematopoietic Cells in Nude Beige Recipients

Abstract

CS7BL/6J (B6) mice homozygous for the viable motheaten (me*) mutation are short-lived and display severe immunodeficiency, autoimmunity and inflammatory disease. B6 mice doubly homozygous for the nude (nu) and beige (bg) mutations (nubg mice) are also short-lived and immunodeficient. Nevertheless, grafts of me^v lympho-hematopoietic cells increased life expectancy of nubg recipients. Such [me^v → nubg] chimeras did not develop any me^v-Mike inflammatory pathology but showed autoimmunity 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 host B-cell origin of the IgG2a overproduced by these chimeras. Yet, about half of such chimera serum IgM being IgM^b, me^v B cells had actually 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 dysfunctions.

Key Words:

• Viable motheaten syndrome
• B-cell abnormality
• nude beige recipients
• adoptive transfer