Stuge Tor B, Skogen Bjørn, Ahlen Maria Therese, Husebekk Anne, Urbaniak Stanislaw J, Bessos Hagop
Laboratory Medicine, University Hospital of North Norway, Tromsø, Norway.
Transfus Apher Sci. 2011 Aug;45(1):53-9. doi: 10.1016/j.transci.2011.06.003. Epub 2011 Jun 25.
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.
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。