Genetic dissection of immunity in leprosy

被引：64

作者：

Alcaïs, A

Mira, M

Casanova, JL

Schurr, E

Abel, L ^{[1
]}

机构：

[1] Univ Paris 05, INSERM U 550, Fac Med Necker, Lab Genet Humaine Malad Infect, Paris, France

[2] McGill Univ, McGill Ctr Study Host Resistance, Montreal, PQ H3A 2T5, Canada

[3] McGill Univ, Dept Human Genet, Montreal, PQ H3A 2T5, Canada

[4] McGill Univ, Dept Med, Montreal, PQ H3A 2T5, Canada

[5] McGill Univ, Dept Biochem, Montreal, PQ H3A 2T5, Canada

[6] Pontificia Univ Catolica Parana, Programa Grad Ciencias Saude, Curitiba, Parana, Brazil

[7] Hop Necker Enfants Malad, Unite Immunol & Hematol, Paris, France

来源：

CURRENT OPINION IN IMMUNOLOGY | 2005年 / 17卷 / 01期

关键词：

D O I：

10.1016/j.coi.2004.11.006

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Leprosy is a chronic infectious disease caused by Mycobacterium leprae that affects an estimated 700 000 new individuals each year. A strong contribution of host genetics to susceptibility to leprosy has long been suggested to account for the considerable variability observed between individuals exposed to M. leprae. As there is no relevant animal model for human leprosy, forward genetics is the main strategy used to identify the genes and, consequently, the immunological pathways involved in protective immunity to M. leprae. With respect to genome-wide screens, a major breakthrough has been reported this year; variants in the regulatory region shared by PARK2 and PACRG have been identified as being common risk factors for leprosy.

引用

页码：44 / 48

页数：5

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