Development of Spontaneous Autoimmune Peripheral Polyneuropathy in B7-2–Deficient Nod Mice
| Autor: | Stephen D. Miller, Benoît L. Salomon, Hélène Bour-Jordan, Jennifer Arcella, Lesley Rhee, Jeffrey A. Bluestone, Ann M. Girvin, Anthony G. Montag, Honor Hsin, Betty Soliven |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2001 |
| Předmět: |
Aging
peripheral neuropathy T-Lymphocytes Chronic inflammatory demyelinating polyneuropathy Nod Nervous System Autoimmune Disease Experimental Major Histocompatibility Complex Mice 0302 clinical medicine Mice Inbred NOD Ganglia Spinal Immunology and Allergy Medicine NOD mice Mice Knockout 0303 health sciences Membrane Glycoproteins autoimmunity Brain Peripheral Nervous System Diseases Sciatic Nerve 3. Good health medicine.anatomical_structure Organ Specificity Peripheral nervous system Original Article Multiple Sclerosis Immunology Autoimmune Diseases 03 medical and health sciences Antigens CD Ranvier's Nodes Lymphocyte costimulation Immune Tolerance Animals Humans Crosses Genetic 030304 developmental biology Inflammation Autoimmune disease business.industry Nervous tissue animal model medicine.disease Peripheral neuropathy Diabetes Mellitus Type 1 B7-2 costimulation Commentary B7-2 Antigen business 030215 immunology |
| Zdroj: | The Journal of Experimental Medicine |
| ISSN: | 1540-9538 0022-1007 |
| Popis: | An increasing number of studies have documented the central role of T cell costimulation in autoimmunity. Here we show that the autoimmune diabetes-prone nonobese diabetic (NOD) mouse strain, deficient in B7-2 costimulation, is protected from diabetes but develops a spontaneous autoimmune peripheral polyneuropathy. All the female and one third of the male mice exhibited limb paralysis with histologic and electrophysiologic evidence of severe demyelination in the peripheral nerves beginning at 20 wk of age. No central nervous system lesions were apparent. The peripheral nerve tissue was infiltrated with dendritic cells, CD4+, and CD8+ T cells. Finally, CD4+ T cells isolated from affected animals induced the disease in NOD.SCID mice. Thus, the B7-2–deficient NOD mouse constitutes the first model of a spontaneous autoimmune disease of the peripheral nervous system, which has many similarities to the human disease, chronic inflammatory demyelinating polyneuropathy (CIDP). This model demonstrates that NOD mice have “cryptic” autoimmune defects that can polarize toward the nervous tissue after the selective disruption of CD28/B7-2 costimulatory pathway. |
| Databáze: | OpenAIRE |
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