Induction of autoimmunity by pristane and other naturally occurring hydrocarbons

被引:287
作者
Reeves, Westley H. [1 ]
Lee, Pui Y. [1 ]
Weinstein, Jason S. [1 ]
Satoh, Minoru [1 ]
Lu, Li [2 ]
机构
[1] Univ Florida, Div Clin Immunol & Rheumatol, Gainesville, FL 32610 USA
[2] Univ Florida, Dept Pathol Immunol & Lab Med, Gainesville, FL 32610 USA
关键词
SYSTEMIC-LUPUS-ERYTHEMATOSUS; PLASMACYTOID DENDRITIC CELLS; IMMUNE-COMPLEX GLOMERULONEPHRITIS; INDUCIBLE GENE-EXPRESSION; I INTERFERON; MINERAL-OIL; BALB/C MICE; RHEUMATOID-ARTHRITIS; B-CELLS; GERMINAL-CENTERS;
D O I
10.1016/j.it.2009.06.003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Tetra methylpentadecane (TMPD, or commonly known as pristane)-induced lupus is a murine model of systemic lupus erythematosus (SLIE). Renal disease and autoantibody production strictly depend on signaling through the interferon (IFN)-I receptor. The major source of IFN-I is immature monocytes bearing high levels of the surface marker Ly6C. Interferon production is mediated exclusively by signaling through TLR7 and the adapter protein MyD88. It is likely that endogenous TLR7 ligands such as components of small nuclear ribonucleoprotein complexes are involved in triggering disease. Lupus autoantilbodies are produced in ectopic lymphoid tissue developing in response to TMPD. This model is well suited for examining links between dysregulated IFN-I production and the pathogenesis of human SLE, which like TMPD-lupus, is associated with high levels of IFN-I.
引用
收藏
页码:455 / 464
页数:10
相关论文
共 96 条
[1]   Lymphoid neogenesis in chronic inflammatory diseases [J].
Aloisi, F ;
Pujol-Borrell, R .
NATURE REVIEWS IMMUNOLOGY, 2006, 6 (03) :205-217
[2]   INDUCTION OF PLASMA CELL TUMOURS IN BALB/C MICE WITH 2,6,10,14-TETRAMETHYLPENTADECANE (PRISTANE) [J].
ANDERSON, PN ;
POTTER, M .
NATURE, 1969, 222 (5197) :994-&
[3]  
AVIGAN J, 1968, J LIPID RES, V9, P350
[4]   Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus [J].
Baechler, EC ;
Batliwalla, FM ;
Karypis, G ;
Gaffney, PM ;
Ortmann, WA ;
Espe, KJ ;
Shark, KB ;
Grande, WJ ;
Hughes, KM ;
Kapur, V ;
Gregersen, PK ;
Behrens, TW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (05) :2610-2615
[5]   Type I interferon in systemic lupus erythematosus and other autoimmune diseases [J].
Banchereau, Jacques ;
Pascual, Virginia .
IMMUNITY, 2006, 25 (03) :383-392
[6]   Nucleic acids of mammalian origin can act as endogenous ligands for toll-like receptors and may promote systemic lupus erythematosus [J].
Barrat, FJ ;
Meeker, T ;
Gregorio, J ;
Chan, JH ;
Uematsu, S ;
Akira, S ;
Chang, B ;
Duramad, O ;
Coffman, RL .
JOURNAL OF EXPERIMENTAL MEDICINE, 2005, 202 (08) :1131-1139
[7]   FcγRIIa is expressed on natural IFN-α-producing cells (plasmacytoid dendritic cells) and is required for the IFN-α production induced by apoptotic cells combined with lupus IgG [J].
Båve, U ;
Magnusson, M ;
Eloranta, ML ;
Perers, A ;
Alm, GV ;
Rönnblom, L .
JOURNAL OF IMMUNOLOGY, 2003, 171 (06) :3296-3302
[8]  
Beech JT, 1997, BRIT J RHEUMATOL, V36, P1129
[9]  
BENECH P, 1985, NUCLEIC ACIDS RES, V13, P1267
[10]   Interferon and granulopoiesis signatures in systemic lupus erythematosus blood [J].
Bennett, L ;
Palucka, AK ;
Arce, E ;
Cantrell, V ;
Borvak, J ;
Banchereau, J ;
Pascual, V .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (06) :711-723