T cell repertoire formation and molecular mimicry in rheumatoid arthritis.

T cell repertoire formation and molecular mimicry in rheumatoid arthritis.
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类风湿关节炎中 T 细胞库的形成和分子模拟。

DOI:
10.1159/000060513
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发表时间:
2001
期刊:
Current directions in autoimmunity.
影响因子:
--
通讯作者:
Albani,S
Albani,S
中科院分区:
--
文献类型:
--
作者:
Prakken,BJ;Carson,DA;Albani,S

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During millions of years of evolution, the human immune system has evolved together with microorganisms in the environment, leading to a dynamic and delicate balance of cohabitation. The healthy immune system consists of a complex network of interacting antigen-specific and nonspecific cells, capable of fulfilling a triad of functions, namely recognition of the danger, action and memory. T cells are central in the regulation of the immune system and mediate specific cellular immune responses. A mature T cell recognizes an antigen presented to it as peptide fragments bound to major histocompatibility complex (MHC) molecules on an antigen-presenting cell (APC) in the context of different costimulatory molecules [1, 2]. T cells originate from progenitor cells in the bone marrow, and migrate to the thymus where they differentiate into mature effector T cells, after undergoing positive selection. One of the most intriguing characteristics of the immune system is its specificity; when threatened by a potential dangerous invading microorganism, the immune system mounts a specific immune response tailored to eliminating the challenge, without causing harm to itself. For years it was thought that the immune system primarily achieves this by differentiating between self and nonself. According to this theory, all self-reactive cells are deleted when undergoing thymic selection, resulting in an adult immune system that does not react to any self antigen, and that recognizes and eliminates any nonself structure, such as foreign antigens. However, with the growing knowledge of immunology, this theory has become more and more unsatisfactory.
热休克蛋白是否控制炎症性疾病中 T 细胞调节的平衡?
DOI: 10.1016/s0167-5699(98)01283-3
发表时间: 1998
期刊: Immunology today
影响因子: --
作者:
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发表时间: 1997
期刊: Autoimmunity
影响因子: 3.5
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