Time for a gut check: evidence for the hypothesis that HLA-B27 predisposes to ankylosing spondylitis by altering the microbiome.
Time for a gut check: evidence for the hypothesis that HLA-B27 predisposes to ankylosing spondylitis by altering the microbiome.
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DOI：
10.1002/art.30558
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发表时间：
2011-11
影响因子：
--
通讯作者：
Davey, Michael P.
中科院分区：
文献类型：
--
作者：
Rosenbaum, James T.;Davey, Michael P.
Nearly four decades have passed since two groups first reported the remarkable relationship between HLA B27 and ankylosing spondylitis 1, 2. This is arguably the strongest association between a genetically determined factor and a genetically complex, immune-mediated disease. The more technologically sophisticated approach through genome wide scanning tends to discover genes that are two orders of magnitude less influential in predisposing to a disease compared to the effect of B27. And equally remarkable as the discovery of the B27-ankylosing spondylitis relationship is the frustrating observation that we are still unable to determine precisely the mechanism of this biological effect.A recent report on an international workshop on the role of HLA B27 in spondyloarthritis summarizes three leading theories as to why HLA B27 predisposes to inflammation: a) HLA B27 presents a distinct peptide repertoire and thus has a direct effect on the immune response as would be expected by an MHC molecule; b) HLA B27 misfolds and activates a series of intracellular events known as the unfolded protein response; c) HLA B27 forms a dimer on the cell surface and this serves as a target for NK cells. 3. None of these theories, however, adequately explains the pathogenesis of spondyloarthropathy. This summary 3 of the proceedings of a meeting sponsored by the National Institute of Arthritis and Musculoskeletal Diseases for members of IGAS (International Genetics of Ankylosing Spondylitis), SPARTAN (Spondylitis Research and Therapy Network), as well as interested members of PANLAR (PanAmerican League Against Rheumatism), does not include mention of the role of endogenous flora in the pathogenesis of this disease.
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影响因子：
64.8
作者：
通讯作者：
--
DOI：
10.1126/science.1198469
发表时间：
2011-01-21
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Atarashi K;Tanoue T;Shima T;Imaoka A;Kuwahara T;Momose Y;Cheng G;Yamasaki S;Saito T;Ohba Y;Taniguchi T;Takeda K;Hori S;Ivanov II;Umesaki Y;Itoh K;Honda K
通讯作者：
Honda K
影响因子：
64.8
作者：
Arumugam, Manimozhiyan;Raes, Jeroen;Pelletier, Eric;Le Paslier, Denis;Yamada, Takuji;Mende, Daniel R.;Fernandes, Gabriel R.;Tap, Julien;Bruls, Thomas;Batto, Jean-Michel;Bertalan, Marcelo;Borruel, Natalia;Casellas, Francesc;Fernandez, Leyden;Gautier, Laurent;Hansen, Torben;Hattori, Masahira;Hayashi, Tetsuya;Kleerebezem, Michiel;Kurokawa, Ken;Leclerc, Marion;Levenez, Florence;Manichanh, Chaysavanh;Nielsen, H. Bjorn;Nielsen, Trine;Pons, Nicolas;Poulain, Julie;Qin, Junjie;Sicheritz-Ponten, Thomas;Tims, Sebastian;Torrents, David;Ugarte, Edgardo;Zoetendal, Erwin G.;Wang, Jun;Guarner, Francisco;Pedersen, Oluf;de Vos, Willem M.;Brunak, Soren;Dore, Joel;Weissenbach, Jean;Ehrlich, S. Dusko;Bork, Peer
通讯作者：
Bork, Peer
影响因子：
15.9
作者：
Abdollahi-Roodsaz, Shahla;Joosten, Leo A. B.;Van den Berg, Wim B.
通讯作者：
Van den Berg, Wim B.
健康，慢病毒感染和慢性小肠结肠炎的猕猴肠道微生物组。
影响因子：
6.7
作者：
McKenna P;Hoffmann C;Minkah N;Aye PP;Lackner A;Liu Z;Lozupone CA;Hamady M;Knight R;Bushman FD
通讯作者：
Bushman FD