Humoral and Cellular Autoimmune Responses in Stiff Person Syndrome
العنوان: | Humoral and Cellular Autoimmune Responses in Stiff Person Syndrome |
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المؤلفون: | R. David G. Leslie, Marco Londei, Tobias Lohmann, Mohammed I. Hawa |
المصدر: | Annals of the New York Academy of Sciences. 998:215-222 |
بيانات النشر: | Wiley, 2003. |
سنة النشر: | 2003 |
مصطلحات موضوعية: | Adult, Male, endocrine system, Adolescent, endocrine system diseases, T-Lymphocytes, T cell, Autoimmunity, Stiff-Person Syndrome, Human leukocyte antigen, In Vitro Techniques, General Biochemistry, Genetics and Molecular Biology, Epitope, Immune system, History and Philosophy of Science, Antigen, Antibody Specificity, medicine, Humans, Child, Aged, Autoimmune disease, Immunity, Cellular, biology, Glutamate Decarboxylase, Immunodominant Epitopes, business.industry, General Neuroscience, nutritional and metabolic diseases, Middle Aged, medicine.disease, Peptide Fragments, Isoenzymes, Diabetes Mellitus, Type 1, medicine.anatomical_structure, Case-Control Studies, Child, Preschool, Antibody Formation, Immunology, biology.protein, Female, Antibody, business, Stiff person syndrome |
الوصف: | Stiff person syndrome (SPS) is a chronic autoimmune disease associated with humoral and cellular immune responses to glutamic acid decarboxylase (GAD) 65. Another chronic autoimmune disease, type 1 diabetes (T1D), is also associated with autoimmune responses to this antigen, but T1D patients develop SPS only extremely rarely and only a third of SPS patients develop T1D (mostly mild manifestations in adulthood). In a previous study, we described important differences between T1D and SPS in the autoimmune response to GAD 65: (1) T cells of SPS patients recognize epitopes in the middle of GAD 65 (amino residues 81–171 and 313–403), whereas patients with T1D preferentially recognize another middle (161–243) and a C-terminal region (473–555); and (2) GAD antibodies (Abs) were nearly exclusively of the Th1-associated IgG1 type in T1D, whereas SPS patients had both Th1- and Th2-associated IgG4 and IgE GAD Abs. These differences were not simply related to different HLA alleles. Fine epitope mapping revealed further distinct T cell epitopes in both diseases despite similar HLA background. Therefore, a single autoantigen can elicit different immune responses causing distinct chronic autoimmune diseases possibly related to a Th1 or Th2 bias of the disease. |
تدمد: | 1749-6632 0077-8923 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a37fa9fffbc1861f94d82d6854f0faffTest https://doi.org/10.1196/annals.1254.024Test |
حقوق: | CLOSED |
رقم الانضمام: | edsair.doi.dedup.....a37fa9fffbc1861f94d82d6854f0faff |
قاعدة البيانات: | OpenAIRE |
تدمد: | 17496632 00778923 |
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