CD36 deficiency is frequent and can cause platelet immunization in Africans

被引:64
作者
Lee, K
Godeau, B
Fromont, P
Plonquet, A
Debili, N
Bachir, D
Reviron, D
Gourin, J
Fernandez, E
Galactéros, F
Bierling, P
机构
[1] Hop Henri Mondor, Ctr Blood, Platelet Immunol Lab, F-94010 Creteil, France
[2] Hop Henri Mondor, Immunol Lab, Sickle Cell Ctr, F-94010 Creteil, France
[3] Inst Gustave Roussy, INSERM, U362, F-94805 Villejuif, France
[4] Ctr Blood, Marseille, France
[5] Ctr Blood, Ajaccio, France
关键词
D O I
10.1046/j.1537-2995.1999.39080873.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND : 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. STUDY DESIGN AND METHODS :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. RESULTS : 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-CD3B. 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. CONCLUSION : 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.
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页码:873 / 879
页数:7
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