کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6369768 1623835 2015 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Autoantigen complementarity and its contributions to hallmarks of autoimmune disease
ترجمه فارسی عنوان
تکمیلی خودکارآنتیژن و کمک های آن به علائم بیماری های خودایمنی
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک علوم کشاورزی و بیولوژیک (عمومی)
چکیده انگلیسی
The question considered is, “What causes the autoimmune response to begin and what causes it to worsen into autoimmune disease?” The theory of autoantigen complementarity posits that the initiating immunogen causing disease is a protein complementary (antisense) to the self-antigen, rather than a response to the native protein. The resulting primary antibody elicits an anti-antibody response or anti-idiotype, consequently producing a disease-inciting autoantibody. Yet, not everyone who developes self-reactive autoantibodies will manifest autoimmune disease. What is apparent is that manifestation of disease is governed by the acquisition of multiple immune-compromising traits that increase susceptibility and drive disease. Taking into account current cellular, molecular, and genetic information, six traits, or 'hallmarks', of autoimmune disease were proposed: (1) Autoreactive cells evade deletion, (2) Presence of asymptomatic autoantibodies, (3) Hyperactivity of Fc-FcR pathway, (4) Susceptibility to environmental impact, (5) Antigenic modifications of self-proteins, (6) Microbial Infections. Presented here is a discussion on how components delineated in the theory of autoantigen complementarity potentially promote the acquisition of multiple 'hallmarks' of disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Theoretical Biology - Volume 375, 21 June 2015, Pages 88-94
نویسندگان
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