Is FCRL3 a new general autoimmunity gene?

被引:66
作者
Chistiakov, Dimitry A.
Chistiakov, Alexander P.
机构
[1] Univ Pittsburgh, Med Ctr, Dept Pathol, Pittsburgh, PA 15261 USA
[2] Endocrinol Res Ctr, Moscow, Russia
关键词
FCRL3; susceptibility; autoimmunity; rheumatoid arthritis; systemic lupus erythematosus;
D O I
10.1016/j.humimm.2007.01.013
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Autoimmunity is a multistep pathogenic process, which arises in genetically predisposing individuals as a result of the harmful influence of environmental factors causing the breakdown of immune tolerance and induction of self-reactive immune response. Recent findings resolved common pathogenic mechanisms shared between different autoimmune diseases and suggested for the existence of genetic loci that could be involved in general autommunity and hence contribute to susceptibility of several autoimmune diseases. To date, several loci responsible for general autoimmunity have been identified. The Fc receptor-like 3 (FCRL3) gene is one of those loci for which a significant association with a number of autoimmune diseases such as rheumatoid arthritis (RA), autoimmune thyroid disease, and systemic lupus erythematosus (SLE) has been recently shown in Japanese. However, studies in Caucasians failed to confirm a strong association of this gene with RA and SLE and therefore made questionable the putative role of FCRL3 in general autoimmunity. In this review, we discuss whether the FCRL3 gene is a newly discovered gene contributing to shared susceptibility between autoimmune diseases.
引用
收藏
页码:375 / 383
页数:9
相关论文
共 50 条
[41]   Functional haplotypes of PADI4, encoding citrullinating enzyme peptidylarginine deiminase 4, are associated with rheumatoid arthritis [J].
Suzuki, A ;
Yamada, R ;
Chang, XT ;
Tokuhiro, S ;
Sawada, T ;
Suzuki, M ;
Nagasaki, M ;
Nakayama-Hamada, M ;
Kawaida, R ;
Ono, M ;
Ohtsuki, M ;
Furukawa, H ;
Yoshino, S ;
Yukioka, M ;
Tohma, S ;
Matsubara, T ;
Wakitani, S ;
Teshima, R ;
Nishioka, Y ;
Sekine, A ;
Iida, A ;
Takahashi, A ;
Tsunoda, T ;
Nakamura, Y ;
Yamamoto, K .
NATURE GENETICS, 2003, 34 (04) :395-402
[42]   The TRAF6-NFκB signaling pathway in autoimmunity:: not just inflammation [J].
Thomas, R .
ARTHRITIS RESEARCH & THERAPY, 2005, 7 (04) :170-173
[43]   Linkage and interaction of loci on 1q23 and 16q12 may contribute to susceptibility to systemic lupus erythematosus [J].
Tsao, BP ;
Cantor, RM ;
Grossman, JM ;
Kim, SK ;
Strong, N ;
Lau, CS ;
Chen, CJ ;
Shen, N ;
Ginzler, EM ;
Goldstein, R ;
Kalunian, KC ;
Arnett, FC ;
Wallace, DJ ;
Hahn, BH .
ARTHRITIS AND RHEUMATISM, 2002, 46 (11) :2928-2936
[44]   The functional variant-169C/T in the FCRL3 gene does not increase susceptibility to Type 1 diabetes [J].
Turunen, J. A. ;
Wessman, M. ;
Kilpikari, R. ;
Parkkonen, M. ;
Forsblom, C. ;
Groop, P-H. .
DIABETIC MEDICINE, 2006, 23 (08) :925-927
[45]   Genetic association of Fc receptor-like 3 polymorphisms with autoimmune pancreatitis in Japanese patients [J].
Umemura, T. ;
Ota, M. ;
Hamano, H. ;
Katsuyama, Y. ;
Kiyosawa, K. ;
Kawa, S. .
GUT, 2006, 55 (09) :1367-1368
[46]   Lack of association between FCRL3 and FcγRII polymorphisms in Japanese type 1 autoimmune hepatitis [J].
Umemura, Takeji ;
Ota, Masao ;
Yoshizawa, Kaname ;
Katsuyama, Yoshihiko ;
Ichijo, Tetsuya ;
Tanaka, Eiji ;
Kawa, Shigeyuki ;
Kiyosawa, Kendo .
CLINICAL IMMUNOLOGY, 2007, 122 (03) :338-342
[47]   Autoimmune-associated lymphoid tyrosine phosphatase is a gain-of-function variant [J].
Vang, T ;
Congia, M ;
Macis, MD ;
Musumeci, L ;
Orrú, V ;
Zavattari, P ;
Nika, K ;
Tautz, L ;
Taskén, K ;
Cucca, F ;
Mustelin, T ;
Bottini, N .
NATURE GENETICS, 2005, 37 (12) :1317-1319
[48]   A novel polymorphic CAAT/enhancer-binding protein β element in the FasL gene promoter alters Fas ligand expression:: A candidate background gene in African American systemic lupus erythematosus patients [J].
Wu, JM ;
Metzt, C ;
Xu, XL ;
Abe, R ;
Gibson, AW ;
Edberg, JC ;
Cooke, J ;
Xie, FL ;
Cooper, GS ;
Kimberly, TP .
JOURNAL OF IMMUNOLOGY, 2003, 170 (01) :132-138
[49]   SPAP2, an Ig family receptor containing both ITIMs and ITAMs [J].
Xu, MJ ;
Zhao, RX ;
Cao, HX ;
Zhao, ZZJ .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2002, 293 (03) :1037-1046
[50]  
Zoller KE, 1997, J IMMUNOL, V158, P1650