Lee K, Godeau B, Fromont P, Plonquet A, Debili N, Bachir D, Reviron D, Gourin J, Fernandez E, Galactéros F, Bierling P
Blood Center, Henri Mondor Hospital, Creteil, France.
Transfusion. 1999 Aug;39(8):873-9. doi: 10.1046/j.1537-2995.1999.39080873.x.
CD36 is expressed on several cell lineages. About 5 to 10 percent of Asians lack platelet membrane CD36 (pCD36), but the frequency of pCD36 deficiency in other ethnic groups is not known. Persons who are pCD36-negative are apparently healthy but can develop CD36 isoimmunization.
The pCD36 phenotype was studied in 1885 subjects belonging either to a group of 1127 healthy French blood donors (almost all of whom were white Europeans) or to a group of 758 patients of known ethnic origin.
No pCD36-negative persons were found among the blood donors. Only 1 of the 301 white European patients was pCD36-negative. In contrast, 16 of the 206 sub-Saharan Africans was pCD36-negative, a proportion higher than that among that black Caribbeans (1/148, p<0.01). The frequency of pCD36-negative patients was similar in blacks with and without sickle cell disease. Monocyte CD36 (mCD36) expression was studied in 15 of 22 pCD36-negative individuals: it was <10 percent in 7 subjects (type I deficiency) and between 12 and 100 percent in 8 others (type II deficiency). Thirteen pCD36-negative individuals had risk factors for immunization, and 4 had anti-CD36. Some had a history resembling posttransfusion purpura (n = 2), platelet transfusion refractoriness (n = 1), and recurrent miscarriage (n = 1). No correlation was found between immunization and the amount of mCD36. Anti-CD36 from an immunized type II-deficient woman reacted with monocytes from normal controls but not with monocytes from type I- or type II-deficient individuals, and thus it is postulated that mCD36 could be structurally different in normal and type II CD36-deficient individuals.
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.
CD36在多种细胞谱系中表达。约5%至10%的亚洲人缺乏血小板膜CD36（pCD36），但其他种族群体中pCD36缺乏的频率尚不清楚。pCD36阴性的人表面上健康，但可能会发生CD36同种免疫。
对1885名受试者的pCD36表型进行了研究，这些受试者要么属于1127名健康法国献血者群体（几乎全是白种欧洲人），要么属于758名已知种族来源的患者群体。
在献血者中未发现pCD36阴性的人。301名白种欧洲患者中只有1人pCD36阴性。相比之下，206名撒哈拉以南非洲人中有16人pCD36阴性，这一比例高于加勒比黑人（1/148，p<0.01）。患与未患镰状细胞病的黑人中pCD36阴性患者的频率相似。在22名pCD36阴性个体中的15名中研究了单核细胞CD36（mCD36）表达：7名受试者中mCD36表达<10%（I型缺乏），另外8名受试者中mCD36表达在12%至100%之间（II型缺乏）。13名pCD36阴性个体有免疫风险因素，4人有抗CD36。一些人有类似输血后紫癜的病史（n = 2）、血小板输注无效（n = 1）和反复流产（n = 1）。未发现免疫与mCD36量之间的相关性。一名免疫的II型缺乏女性的抗CD36与正常对照的单核细胞反应，但不与I型或II型缺乏个体的单核细胞反应，因此推测正常人和II型CD36缺乏个体中的mCD36在结构上可能不同。
CD36缺乏在撒哈拉以南非洲人中很常见；抗CD36的产生可导致多次输血患者（如镰状细胞病患者）出现严重并发症。
