HLA-DP control of human Schistosoma haematobium infection

被引:16
作者
May, J
Kremsner, PG
Milovanovic, D
Schnittger, L
Löliger, CC
Bienzle, U
Meyer, CG
机构
[1] Humboldt Univ, Inst Trop Med, D-14050 Berlin, Germany
[2] Humboldt Univ, Med Fak Charite, D-14050 Berlin, Germany
[3] Univ Tubingen, Inst Trop Med, Sekt Humanparasitol, D-72074 Tubingen, Germany
[4] Hop Albert Schweitzer, Lab Rech, Lambarene, Gabon
[5] Univ Hamburg, Hosp Eppendorf, Abt Transfus Med, D-20246 Hamburg, Germany
关键词
D O I
10.4269/ajtmh.1998.59.302
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
The DPA1 and DPB1 alleles of the major histocompatibility complex (MHC) class II were determined in 110 patients and 120 healthy controls of a Gabonese population from an area endemic for Schistosoma haematobium infection. The MHC-DP alleles of the variable second exons and their human leukocyte antigen (HLA) epitopes were correlated with egg excretion, interleukin-4 and interferon-gamma patterns, and bladder abnormalities, as detected by ultrasonography. A methionine at position 11 of the DP alpha molecule (Met-11) and DPA1*0301 were associated with schistosomiasis when compared with controls (phenotypic gene frequencies = 0.791 versus 0.583 and 0.555 versus 0.375, respectively). Met-11 homozygosity occurred more often in patients, whereas healthy controls were more frequently homozygous for an alanine at position 11 (Ala-11). The combination of the DPB1-epitope DEAV (positions 84-87 of the DP beta molecule) and Met-11 positive DPA1 alleles was more frequent in patients than in controls (0.573 versus 0.316). Two years after antischistosomal treatment, the rate of reinfection as examined in 55 of the 110 former patients was higher in DPA1*0301-positive individuals than in those not possessing this allele (P < 0.001). Ala-11 positive individuals showed less frequently ultrasonographic signs of bladder pathology than Ala-11 negative individuals (P < 0.05). Our results suggest a role of MHC-DP elements in the manifestation of disease in S. haematobium infection.
引用
收藏
页码:302 / 306
页数:5
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