Studies of immune responses in mice prone to autoimmune disorders. II. Decreased down-regulation by auto-anti-idiotype antibody in autoimmune-prone mice |
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| Authors: | E A Goidl R A Good G W Siskind M E Weksler G Fernandes |
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| Affiliation: | 1. Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland 21201 USA;2. Department of Microbiology and Immunology, University of Florida, Tampa, Florida, USA;3. Division of Allergy and Immunology, Department of Medicine, Cornell University Medical College, New York, New York 10021 USA;4. Division of Geriatrics and Gerontology, Department of Medicine, Cornell University Medical College, New York, New York 10021 USA;1. Department of Molecular Life Science, Division of Basic Medical Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan;2. Institute of Advanced Biosciences, Tokai University, Hiratsuka, Kanagawa, Japan;3. Department of Breast and Endocrine Surgery, Tokai University School of Medicine, Isehara, Kanagawa, Japan;4. Division of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan;5. Central Institute for Experimental Animals, Kawasaki, Kanagawa, Japan;6. Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan;1. Columbia Center for Translational Immunology, Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA;2. Department of Health Sciences, Histology laboratory, Università del Piemonte Orientale, Novara, Italy;3. Departments of Microbiology & Immunology, and Regenerative Medicine & Cell Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA;4. Department of Pathology, Immunology and Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL, USA;5. Program in Molecular Medicine, Diabetes Center of Excellence, University of Massachusetts Medical School, Worcester, MA, USA;6. Diabetes Center, University of California San Francisco, San Francisco, CA, USA;1. Chronic Disease Laboratory, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, 510006, China;2. Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, Davis, CA, USA;3. Division of Pediatric Immunology and Allergy, Joe DiMaggio Children’s Hospital, Hollywood, FL, USA |
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| Abstract: | Three lines of evidence are presented which suggest that autoimmune-prone mice are deficient in the production of auto-anti-idiotype antibody during their immune response to trinitrophenylated Ficoll (TNP-F). NZB, MRL lpr/lpr and older BXSB male mice have no hapten-augmentable plaque-forming cells (PFC). Hapten-augmentable PFC have been previously shown to be cells whose secretion of antibody has been inhibited by the binding of auto-anti-idiotype antibody to cell surface idiotype. Sera from TNP-F immunized NZB mice lack PFC inhibiting activity (anti-idiotype antibody). Spleen cells from TNP-F immune NZB mice fail to transfer anti-idiotype antibody-mediated suppression to naive mice as do spleen cells from immune non-autoimmune-prone mice. Taken together these data suggest that autoimmune-prone mice are deficient in auto-anti-idiotype antibody-mediated downward regulation of their immune responses. It was further shown that the immune response of NZB mice to TNP-F shows a slower decline in splenic PFC and a greater heterogeneity of PFC affinity than do the responses of non-autoimmune-prone strains. Since athymic (nude) mice, which were previously shown to be defective in the production of auto-anti-idiotype antibody, also show a slower decline in splenic PFC and an increased heterogeneity of PFC affinity, it is suggested that these peculiarities of the immune responses of autoimmune-prone and athymic mice are also the consequences of the lack of auto-anti-idiotype antibody-mediated down-regulation. |
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