生物谷报道：类风湿性关节炎的发病与多种细胞因子如TNF-α、IL-1、IL-17等有关。IL-17是一种前炎症细胞因子，在活动性类风湿性关节炎患者血清及关节液中的表现量均会增高。
IL-17主要由活化的T细胞所制造，会诱导活化T细胞、促进滑膜细胞分泌多种细胞因子、抑制软骨细胞合成基质、增强破骨细胞活性，最后会导致骨侵蚀。
IL-17可以与其它细胞因子产生交互作用，导致类风湿性关节炎进一步发展。IL-17在类风湿性关节炎进程中起重要的调节作用,因此抗IL-17抗体生物治疗有望成为治疗类风湿性关节炎的新方法。
根据水牛城大学的研究人员发表的研究，证实这种会破坏骨头并导致自体免疫疾病之发炎情况的因子IL-17，可以保护口腔中的骨头免于受到病原菌如Porphyromonas gingivalis感染，这是造成牙周病的主因。
(资料来源 : Bio.com)
英文原文：
原始出处:
Blood, 1 May 2007, Vol. 109, No. 9, pp. 3794-3802.
Prepublished online as a Blood First Edition Paper on January 3, 2007; DOI 10.1182/blood-2005-09-010116.
IMMUNOBIOLOGY
An essential role for IL-17 in preventing pathogen-initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor–dependent signals
Jeffrey J. Yu1, Matthew J. Ruddy1, Grace C. Wong2, Cornelia Sfintescu2, Pamela J. Baker3, Jeffrey B. Smith4, Richard T. Evans2, and Sarah L. Gaffen1,2
1 Department of Microbiology and Immunology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY; 2 Department of Oral Biology, School of Dental Medicine, University at Buffalo, SUNY, Buffalo NY; 3 Department of Biology, Bates College, Lewiston ME; 4 Department of Pediatrics, David Geffen School of Medicine and Mattel Children's Hospital at University of California at Los Angeles, Los Angeles, CA
IL-17 and its receptor are founding members of a novel family of inflammatory cytokines. IL-17 plays a pathogenic role in rheumatoid arthritis (RA)–associated bone destruction. However, IL-17 is also an important regulator of host defense through granulopoiesis and neutrophil trafficking. Therefore, the role of IL-17 in pathogen-initiated bone loss was not obvious. The most common form of infection-induced bone destruction occurs in periodontal disease (PD). In addition to causing significant morbidity, PD is a risk factor for atherosclerotic heart disease and chronic obstructive pulmonary disease (COPD). Similar to RA, bone destruction in PD is caused by the immune response. However, neutrophils provide critical antimicrobial defense against periodontal organisms. Since IL-17 is bone destructive in RA but a key regulator of neutrophils, we examined its role in inflammatory bone loss induced by the oral pathogen Porphyromonas gingivalis in IL-17RA–deficient mice. These mice showed enhanced periodontal bone destruction, suggesting a bone-protective role for IL-17, reminiscent of a neutrophil deficiency. Although IL-17RA–deficient neutrophils functioned normally ex vivo, IL-17RA knock-out (IL-17RAKO) mice exhibited reduced serum chemokine levels and concomitantly reduced neutrophil migration to bone. Consistently, CXCR2KO mice were highly susceptible to alveolar bone loss; interestingly, these mice also suggested a role for chemokines in maintaining normal bone homeostasis. These results indicate a nonredundant role for IL-17 in mediating host defense via neutrophil mobilization.
