生物谷報(bào)道：類風(fēng)濕性關(guān)節(jié)炎的發(fā)病與多種細(xì)胞因子如TNF-α,、IL-1,、IL-17等有關(guān)。IL-17是一種前炎癥細(xì)胞因子,，在活動(dòng)性類風(fēng)濕性關(guān)節(jié)炎患者血清及關(guān)節(jié)液中的表現(xiàn)量均會(huì)增高,。
IL-17主要由活化的T細(xì)胞所制造,，會(huì)誘導(dǎo)活化T細(xì)胞,、促進(jìn)滑膜細(xì)胞分泌多種細(xì)胞因子、抑制軟骨細(xì)胞合成基質(zhì),、增強(qiáng)破骨細(xì)胞活性,，最后會(huì)導(dǎo)致骨侵蝕。
IL-17可以與其它細(xì)胞因子產(chǎn)生交互作用,，導(dǎo)致類風(fēng)濕性關(guān)節(jié)炎進(jìn)一步發(fā)展,。IL-17在類風(fēng)濕性關(guān)節(jié)炎進(jìn)程中起重要的調(diào)節(jié)作用,因此抗IL-17抗體生物治療有望成為治療類風(fēng)濕性關(guān)節(jié)炎的新方法,。
根據(jù)水牛城大學(xué)的研究人員發(fā)表的研究，證實(shí)這種會(huì)破壞骨頭并導(dǎo)致自體免疫疾病之發(fā)炎情況的因子IL-17,，可以保護(hù)口腔中的骨頭免于受到病原菌如Porphyromonas gingivalis感染,，這是造成牙周病的主因。
(資料來源 : Bio.com)
英文原文：
原始出處:
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.
