生物谷報(bào)道：來自布法羅大學(xué)的研究報(bào)告稱：在骨降解和自身免疫疾病的炎癥中有著重要地位的一個(gè)免疫系統(tǒng)組分（immune system component），在保護(hù)著口腔免受傳染病病原體的侵害，而這種病原體卻是人類牙周?。╬eriodontal diseas）的主要誘因,。
這個(gè)免疫系統(tǒng)組分是IL-17，在過去的18個(gè)月期間，被識別出在骨降解和自身免疫疾病的炎癥中是主要誘導(dǎo)分子。針對IL-17或它的細(xì)胞受體的療法日前正在不斷開發(fā)出來。
但是,，布法羅大學(xué)的一名生物學(xué)家卻發(fā)現(xiàn)，與該分子在類風(fēng)濕性關(guān)節(jié)炎中的行為不同,，IL-17卻“反其道而行之”地保護(hù)著口腔免受傳染病病原體的侵害,，如牙齦卟啉菌（Porphyromonas gingivalis），該病菌是人類牙周病的主要誘因,。
該研究發(fā)表在5月期的《血液》（Blood）雜志上,。
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
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
Abstract
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.
