一項研究認為,，懷疑能夠保護亞洲和非洲裔不受瘧疾影響的一個基因變種可能增加這些人對狼瘡的易感性,。
Kenneth Smith及其同事對從肯尼亞,、香港和英國征集的將近5000位狼瘡和瘧疾患者進行了基因分型,，并搜尋了受試者DNA的FCGR2B基因的一個變種，已知該基因變種在亞洲人和撒哈拉以南非洲人中間更常見,。
此前的研究把這種這個基因的多態(tài)與可能增強狼瘡易感性和瘧疾抗性的一種免疫系統(tǒng)應答聯(lián)系了起來,。這組科學家報告說，香港狼瘡患者的這種FCGR2B多態(tài)比對照組出現(xiàn)得更頻繁,，而患嚴重瘧疾的肯尼亞兒童的這種基因多態(tài)出現(xiàn)的頻率就比一般人群中的肯尼亞兒童更低,。
這些結(jié)果符合已經(jīng)被大家接受的觀察，即與白人相比,，狼瘡在亞裔和非洲裔人群中更加流行,。而且這些結(jié)果可能支持了作者的一種理論，即瘧疾的高死亡率可能驅(qū)動著特定族群的自體免疫疾病易感性的增加,。(生物谷Bioon.com)
生物谷推薦原文出處：
PNAS doi: 10.1073/pnas.0915133107
A defunctioning polymorphism in FCGR2B is associated with protection against malaria but susceptibility to systemic lupus erythematosus
Lisa C. Willcocksa, Edward J. Carra, Heather A. Niederera, Tim F. Raynera, Thomas N. Williamsb,c,d,e, Wanling Yangf, J. Anthony G. Scottb,c, Britta C. Urbanb,g, Norbert Peshub, Timothy J. Vyseh, Yu Lung Lauf, Paul A. Lyonsa, and Kenneth G. C. Smitha,1
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease more prevalent in people of African and Asian origin than Caucasian origin. FcγRIIb is an inhibitory Fc receptor with a critical role in immune regulation. Mouse data suggest that FcγRIIb deficiency increases susceptibility to autoimmune disease but protects against infection. We show that a SNP in human FCGR2B that abrogates receptor function is strongly associated with susceptibility to SLE in both Caucasians and Southeast Asians. The minor allele of this SNP is more common in Southeast Asians and Africans, populations from areas where malaria is endemic, than in Caucasians. We show that homozygosity for the minor allele is associated with substantial protection against severe malaria in an East African population (odds ratio = 0.56; P = 7.1 × 10(5)). This protective effect against malaria may contribute to the higher frequency of this SNP and hence, SLE in Africans and Southeast Asians.
