STUDIES OF CONGENITALLY IMMUNOLOGICAL MUTANT NEW-ZEALAND MICE .2. ABSENCE OF T-CELL PROGENITOR POPULATIONS AND B-CELL DEFECTS OF CONGENITALLY ATHYMIC (NUDE) NEW-ZEALAND BLACK (NZB) MICE

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  • 1 January 1979
    • journal article
    • research article
    • Vol. 122  (5) , 2020-2025
Abstract
Congenitally athymic (nude) mice on an NZB, NZW, and BALB/c background were produced by repetitive selective backcrossing. F12 generation nude mice of these 3 strains were compared to their littermate nu/+ controls with respect to survival, histology, blood counts, splenic surface markers, response to mitogens, spontaneous plaque-forming cells and appearance of naturally occurring thymocytotoxic antibodies (NTA). Under specific pathogen-free conditions, NZB nude mice survived less than 3 wk, dying of a runting-like disease with infection by local normally noninvasive organisms. A contributing factor to this premature death is the relative absence of T [thymus-derived] cell progenitor populations in the NZB nude vs. NZW nude or BALB/c nude groups. NZB nude mice had a significantly earlier appearance of NTA than nu/+ littermates and appeared to have heightened spontaneous polyclonal B [bone marrow-derived] cell responses against the haptens dansyl, nitroiodophenyl, trinitrophenyl, 2,4-dinitrophenyl and sulfonate. NZB mice apparently have several critical immunologic defects, including abnormalities of thymic epithelial cells, T cell differentiation pathways and chronically polyclonal activated B cell populations. The defects interact to produce the clinical expression of autoimmunity.