Mechanisms that Modify Immune Response in Neonatal Alloimmune Thrombocytopenia

Authors

Robert Cooper, Department of Pathology, Anatomy & Cell Biology, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PAFollow
Jay H. Herman, Department of Pathology, Anatomy & Cell Biology, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PAFollow

Document Type

Poster

Publication Date

6-2014

Abstract

What is NAIT?

Neonatal alloimmune thrombocytopenia (NAIT) is a form of fetal and neonatal thrombocytopenia caused by maternal-fetal platelet antigen incompatibility that results in placental transfer of maternal IgG alloantibodies against the platelet antigen. Currently, there are 28 human platelet antigen systems (HPA) that are polymorphisms of various membrane glycoprotein (GP) integrins. The first HPA and most immunogenic was discovered in the 1960’s and is now termed HPA-1, a diallelic system with HPA-1a and HPA-1b on the GPβ3 subunit of the fibrinogen receptor (Murphy). Approximate HPA-1 phenotype frequencies are: homozygous 1a,1a (~70%); heterozygous 1a,1b (~28%); homozygous 1b,1b (~2%).

Typically an HPA-1a negative mother (HPA-1b,1b) can develop antibodies against the HPA-1a antigen passed on to the fetus by an HPA-1a positive father. NAIT due to anti-HPA-1a often causes severe thrombocytopenia, responsible for both antenatal as well as post-natal intracranial hemorrhage (ICH) in approximately 26% of affected fetuses/neonates, as well as post-natal hemorrhage and purpura/petechiae of variable severity. ICH is the major cause of morbidity and mortality in NAIT causing blindness, significant physical and mental disability, and is fatal in 7% of affected neonates (Murphy).

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