Titlebook: Current Concepts in Autoimmunity and Chronic Inflammation; Andreas Radbruch,Peter E. Lipsky Book 2006 The Editor(s) (if applicable) and Th

Musculoskeletal

Signalling Pathways in B Cells: Implications for Autoimmunity,of B cells in the maintenance of the disease process beyond just being precursors of (auto)antibody-producing plasma cells. Detailed analyses have implicated a number of surface molecules and subsequent downstream signalling pathways in the regulation of the events induced by BCR engagement. In this

Carcinoma

folliculitis

節(jié)省

Dappled

Conclusions: Loss, Trauma, Recovery,toantigen in the thymus or in the periphery and active suppression by regulatory cells. A third way to prevent autoimmunity is by hiding self tissues behind a tissue barrier impermeable for circulating immune cells. The latter mechanism has been held responsible for self-tolerance within the nervous

除草劑

Tremor

Chi Han Chen,Bo Han Chen,Anthony Y. Changhave been conducted. While it is plausible that some sex-linked genes may contribute to the genetic predisposition for the disease, other likely culprits are the sex hormones estrogen and prolactin. In this chapter we review studies that have addressed the influence of sex hormones in SLE activity a

gruelling

https://doi.org/10.1007/978-3-030-52988-8ue. Here we discuss that autoimmune disease is often preceded by autoreactivity, meaning the priming of autoantigen-specific immune cells without relevant tissue damage. Recent experimental evidence has demonstrated that both the induction of autoreactivity and the conversion into autoimmune disease

MORPH

Chien-Liang Chen,Ding-Jung Chiangcular emphasis on Crohn’s disease and ankylosing spondylitis. Direct proof that infection establishes persistent autoimmunity remains lacking, although it may provoke a prolonged inflammatory response when occurring on a susceptible immunological background. The argument of infective causality is by

野蠻

Der-Jiunn Deng,Ai-Chun Pang,Chun-Cheng Linacteristic of classic autoimmune disease. Nevertheless, patients with these illnesses experience unprovoked inflammatory disease in the absence of underlying infection. Here we discuss recent advances in eight Mendelian autoinflammatory diseases. The causative genes and the proteins they encode play