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-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. 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.
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-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-deficientwoman 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.
Authors: Alex F Sandes; Mihoko Yamamoto; Sergio Matarraz; Maria de Lourdes L F Chauffaille; Sandra Quijano; Antonio López; Tsutomu Oguro; Eliza Y S Kimura; Alberto Orfao Journal: Haematologica Date: 2012-01-22 Impact factor: 9.941
Authors: Hiroshi Irie; Irvin B Krukenkamp; Joep F F Brinkmann; Glenn R Gaudette; Adam E Saltman; William Jou; Jan F C Glatz; Nada A Abumrad; Azeddine Ibrahimi Journal: Proc Natl Acad Sci U S A Date: 2003-05-13 Impact factor: 11.205
Authors: Tolani F Olonisakin; Huihua Li; Zeyu Xiong; Elizabeth J K Kochman; Minting Yu; Yanyan Qu; Mei Hulver; Jay K Kolls; Claudette St Croix; Yohei Doi; Minh-Hong Nguyen; Robert M Q Shanks; Rama K Mallampalli; Valerian E Kagan; Anuradha Ray; Roy L Silverstein; Prabir Ray; Janet S Lee Journal: J Infect Dis Date: 2016-09-28 Impact factor: 5.226
Authors: Joep F F Brinkmann; Nada A Abumrad; Azeddine Ibrahimi; Ger J van der Vusse; Jan F C Glatz Journal: Biochem J Date: 2002-11-01 Impact factor: 3.857