HLA and Infectious Diseases

被引：262

作者：

Blackwell, Jenefer M. ^{[1
,2
]}

Jamieson, Sarra E. ^{[1
]}

Burgner, David ^{[3
]}

机构：

[1] Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, Perth, WA 6872, Australia

[2] Univ Cambridge, Sch Clin Med, Cambridge Inst Med Res, Addenbrookes Hosp, Cambridge CB2 0XY, England

[3] Univ Western Australia, Princess Margaret Hosp Children, Sch Paediat & Child Hlth, Perth, WA 6840, Australia

来源：

CLINICAL MICROBIOLOGY REVIEWS | 2009年 / 22卷 / 02期

基金：

英国惠康基金;

关键词：

TYPE-1 DIABETES SUSCEPTIBILITY; B-VIRUS INFECTION; LEUKOCYTE ANTIGEN HOMOZYGOSITY; LEISHMANIA-DONOVANI INFECTION; HEPATITIS-B; VISCERAL LEISHMANIASIS; CLASS-II; T-CELLS; IMMUNE-RESPONSES; HETEROZYGOTE ADVANTAGE;

D O I：

10.1128/CMR.00048-08

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Following their discovery in the early 1970s, classical human leukocyte antigen (HLA) loci have been the prototypical candidates for genetic susceptibility to infectious disease. Indeed, the original hypothesis for the extreme variability observed at HLA loci (H-2 in mice) was the major selective pressure from infectious diseases. Now that both the human genome and the molecular basis of innate and acquired immunity are understood in greater detail, do the classical HLA loci still stand out as major genes that determine susceptibility to infectious disease? This review looks afresh at the evidence supporting a role for classical HLA loci in susceptibility to infectious disease, examines the limitations of data reported to date, and discusses current advances in methodology and technology that will potentially lead to greater understanding of their role in infectious diseases in the future.

引用

收藏

页码：370 / +

页数：17

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