Your browser doesn't support javascript.
loading
Recent Advances of Researches on Expression, Function and Regulation of CD22 / 中国实验血液学杂志
Journal of Experimental Hematology ; (6): 573-577, 2015.
Artigo em Chinês | WPRIM | ID: wpr-357313
ABSTRACT
CD22 is a type I transmembrane protein expressed on most mature B lymphocyte, and plays a significant role in signal transduction pathways. CD22 acts as a co-receptor of the B-cell receptor (BCR) that inhibits the BCR signaling by antigen-receptor interaction. The phosphorylation of CD22 can be triggered by cross-linking of CD22 with the BCR through antigen, then predominantly triggers the dephosphorylation and inactivation of downstream proteins and inhibit the BCR signaling. Autoimmune disease could be caused by the abnormal expression or dysfunction of CD22 which interrupts BCR signaling and then influences the quantity and function of B cells. The further study of the function and regulation of CD22 would help us understanding the pathogenesis of autoimmune disease and setting theoretical basis for its targeting treatment. In this article, the structure and expression of CD22, the ligands of CD22, the regulation of BCR and transmenbrane signaling, the effect of CD22 on B cells, and CD22 and autoimmune diseases were reviewed.
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Fosforilação / Doenças Autoimunes / Linfócitos B / Receptores de Antígenos de Linfócitos B / Transdução de Sinais / Lectina 2 Semelhante a Ig de Ligação ao Ácido Siálico Limite: Humanos Idioma: Chinês Revista: Journal of Experimental Hematology Ano de publicação: 2015 Tipo de documento: Artigo

Similares

MEDLINE

...
LILACS

LIS

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Fosforilação / Doenças Autoimunes / Linfócitos B / Receptores de Antígenos de Linfócitos B / Transdução de Sinais / Lectina 2 Semelhante a Ig de Ligação ao Ácido Siálico Limite: Humanos Idioma: Chinês Revista: Journal of Experimental Hematology Ano de publicação: 2015 Tipo de documento: Artigo