Märker-Hermann E, Frauendorf E, Zeidler H, Sieper J
Klinik Innere Medizin IV, Dr. Horst-Schmidt-Kliniken GmbH, Klinikum der Landeshauptstadt Wiesbaden, Aukammallee 39, 65191 Wiesbaden, Germany.
Z Rheumatol. 2004 Jun;63(3):187-92. doi: 10.1007/s00393-004-0628-x.
Despite intensive research during the last three decades, it is still not clear which precise mechanisms determine the interactions between host factors (HLA-B27 and other genes, cytokines, T lymphocytes) and microbial factors leading to the manifestation and chronicity of ankylosing spondylitis (AS). Rheumatologists and histopathologists have focused their interest on decoding the immune-mediated inflammatory processes and on studying new bone formation and ankylosis. Concerning the genetic basis of AS, there is considerable effort in large genome-wide and candidate gene analyses to discover new genes that are associated with AS. Moreover, such genetic studies could identify genomic regions that determine clinical manifestations and the course of disease.
尽管在过去三十年中进行了深入研究,但仍不清楚哪些精确机制决定了宿主因素(HLA - B27和其他基因、细胞因子、T淋巴细胞)与微生物因素之间的相互作用,这些相互作用导致了强直性脊柱炎(AS)的表现和慢性化。风湿病学家和组织病理学家一直致力于解读免疫介导的炎症过程以及研究新骨形成和关节强直。关于AS的遗传基础,在大规模全基因组和候选基因分析方面投入了大量精力,以发现与AS相关的新基因。此外,此类基因研究可以识别决定临床表现和疾病进程的基因组区域。