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与胎儿及新生儿同种免疫性血小板减少症相关的细胞免疫生物学

The cellular immunobiology associated with fetal and neonatal alloimmune thrombocytopenia.

作者信息

Stuge Tor B, Skogen Bjørn, Ahlen Maria Therese, Husebekk Anne, Urbaniak Stanislaw J, Bessos Hagop

机构信息

Laboratory Medicine, University Hospital of North Norway, Tromsø, Norway.

出版信息

Transfus Apher Sci. 2011 Aug;45(1):53-9. doi: 10.1016/j.transci.2011.06.003. Epub 2011 Jun 25.

Abstract

Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is caused by maternal antibodies that cross the placenta in connection with pregnancy and destroy fetal platelets. Recently, maternal T cell responses associated with FNAIT have been studied at the clonal level. These T cell clones recognize an integrin β3 epitope, which is anchored to the HLA-DRB3∗0101-encoded MHC molecule DR52a. The same MHC allele is strongly associated with FNAIT. As the production of pathological antibodies reactive with fetal platelets is likely dependent on these T cell responses, there exists a potential for preventing FNAIT by targeting these T cells.

摘要

胎儿及新生儿同种免疫性血小板减少症(FNAIT)是由孕期穿过胎盘的母体抗体破坏胎儿血小板所致。最近,已在克隆水平研究了与FNAIT相关的母体T细胞反应。这些T细胞克隆识别一种整合素β3表位,该表位锚定在由HLA - DRB3∗0101编码的MHC分子DR52a上。相同的MHC等位基因与FNAIT密切相关。由于与胎儿血小板发生反应的病理性抗体的产生可能依赖于这些T细胞反应,因此存在通过靶向这些T细胞来预防FNAIT的可能性。

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