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Studies of Congenitally Immunologic Mutant New Zealand Mice

II. Absence of T Cell Progenitor Populations and B Cell Defects of Congenitally Athymic (nude) New Zealand Black (NZB) Mice¹

From the Section of Rheumatology-Clinical Immunology, Department of Medicine, and the Department of Anatomy, School of Medicine, University of California, Davis, California 95616, and the National Naval Medical Research Institute, Bethesda, Maryland 20014

Abstract

Congenitally athymic (nude) mice on an NZB, NZW, and BALB/c background were produced by repetitive selective backcrossing. F'₁₂ generation nude mice of these three 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 survive less than 3 weeks, 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 cell progenitor populations in the NZB nude vs NZW nude or BALB/c nude groups. Furthermore, NZB nude mice have a significantly earlier appearance of NTA than nu/+ littermates and likewise appear to have heightened spontaneous polyclonal B cell responses against the haptens dansyl, nitroiodophenyl, trinitrophenyl, 2,4 dinitrophenyl, and sulfonate. It is suggested that NZB mice have several critical immunologic defects, including abnormalities of thymic epithelial cells, T cell differentiation pathways, and chronically polyclonal activated B cell populations. These defects interact to produce the clinical expression of autoimmunity.

Footnotes

¹ This work was supported by National Cancer Institute Grant 20816.

The opinions and assertions contained herein are the private ones of the writers and are not to be construed as official or reflecting the views of the Navy Department or the naval service at large. The experiments reported herein were conducted according to the principles set forth in the "Guide for the Care and Use of Laboratory Animals," Institute of Laboratory Resources, National Research Council, Department of Health, Education and Welfare, Publication No. (National Institutes of Health) 78-23.

² Recipient of Research Career Development Award AI 00193.

³ Correspondence to M. Eric Gershwin, M.D., Section of Rheumatology-Clinical Immunology, TB 192, School of Medicine, University of California, Davis, California 95616.

⁴ Supported by the Naval Medical Research and Development Command, Work Unit No. MR041.02.01.0034.

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