Cases of CD36 deficiency are not rare in Asian populations, foetal and neonatal alloimmune thrombocytopenia (FNAIT) caused by anti-CD36 isoantibodies appears more frequent than other HPA alloantibodies.
In this study, we aimed to detect the expression of CD36 in two different chronic epileptic mouse models and determine whether CD36 deficiency leads to suppressive neuronal hyperexcitability and decreased susceptibility of epileptic seizures.
We found four donors (0·6%) with type I CD36 deficiency (both platelets and monocytes CD36(null) ) and six (1·0%) with type II CD36 deficiency (PLT: CD36(null) , monocyte: CD36(low) ).
A mouse tumor angiogenesis model revealed enhanced PKD-1 signaling and expression of ephrin B2 and smooth muscle actin in neovessels of Lewis Lung Carcinomas, along with low-CD36 expression or CD36 deficiency.
These results demonstrated that the frequencies of Type I (lacking CD36 expression on PLTs and monocytes) and Type II (lacking CD36 expression on PLTs only) CD36 deficiency among the study population were 0.2 and 2.0%, respectively.
A total of 22 variants of the CD36 gene were identified, of which five variants (111 A>T, 681 C>A, 1172-1183 del12b, 1236 delT and 1395 A>C) were novel variations, and nine were also found in single nucleotide polymorphism database (dbSNP) but had not been confirmed in individuals with CD36 deficiency.
The role of CD36 was examined in in vitro studies and in vivo experiments, which investigated various functions of CD36 in atherosclerosis and revealed that CD36 deficiency reduces atherosclerotic lesion formation.
These results suggest a range of possible explanations including the existence of alternative selection pressures on CD36, co-evolution between host and parasite or confounding caused by allelic heterogeneity of CD36 deficiency.
The cumulative data indicate that CD36 facilitates a major fraction of fatty acid uptake by muscle and fat, and that CD36 deficiency is associated with a large (60-80%) defect in fatty acid uptake by those tissues.
To examine the metabolic role of human CD36, we performed a glucose loading test for normals (n = 16) and subjects with CD36 deficiency, both Type I (n = 5) and Type II (n = 16).
CD36 deficiency is frequent in sub-Saharan Africans; development of anti-CD36 can lead to serious complications in multiply transfused patients, such as those with sicke cell disease.