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Erschienen in: Zeitschrift für Rheumatologie 1/2017

31.01.2016 | Neues aus der Forschung

CD22 and CD72 are inhibitory receptors dominantly expressed in B lymphocytes and regulate systemic autoimmune diseases

English version

verfasst von: Prof. Dr. T. Tsubata

Erschienen in: Zeitschrift für Rheumatologie | Sonderheft 1/2017

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Excerpt

B lymphocytes (B cells) express the antigen receptor (B cell receptor: BCR) composed of membrane-bound immunoglobulin and the signal transducing component Igα/Igβ (CD79a/CD79b). When BCR interacts with the antigen, BCR-associated protein tyrosine kinases are activated and trigger cell activation by phosphorylating various signaling molecules. Signaling through BCR plays a crucial role in antibody responses by inducing activation of antigen-stimulated B cells. B cells express various inhibitory receptors that negatively regulate BCR signaling such as FcγRIIB, FCRLs, CD22, Siglec-10/G, CD72, PIR-B, PECAM-1 and PD-1 [1]. Lines of evidence suggest that these inhibitory receptors play a role in prevention of autoimmune diseases including systemic lupus erythematosus (SLE). First, mice deficient in one of these inhibitory receptors often show higher susceptibility to autoimmune disease. Second, polymorphisms of some of these inhibitory receptors associate with autoimmune diseases. The polymorphism of FcγRIIB has been extensively analyzed and was shown to be associated with autoimmune diseases [2]. Although some of the inhibitory receptors are expressed in other immune cell types such as dendritic cells, those such as CD22 and CD72 are dominantly expressed in B cells, and evidence suggests that CD72 regulates autoimmune diseases such as SLE. Thus, inhibition of B cell activation mediated by inhibitory receptors may play a role in prevention of autoimmune diseases. …
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Metadaten
Titel
CD22 and CD72 are inhibitory receptors dominantly expressed in B lymphocytes and regulate systemic autoimmune diseases
English version
verfasst von
Prof. Dr. T. Tsubata
Publikationsdatum
31.01.2016
Verlag
Springer Medizin
Erschienen in
Zeitschrift für Rheumatologie / Ausgabe Sonderheft 1/2017
Print ISSN: 0340-1855
Elektronische ISSN: 1435-1250
DOI
https://doi.org/10.1007/s00393-015-1577-2

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