NDLI: Etude du rôle des homologues de DC-SIGN dans le modèle murin d'infection par Mycobacterium tuberculosis

Please wait, while we are loading the content...

Etude du rôle des homologues de DC-SIGN dans le modèle murin d'infection par Mycobacterium tuberculosis

Content Provider	Semantic Scholar
Author	Tanne, Antoine
Copyright Year	2009
Abstract	Tuberculosis (TB) is due to the infection by Mycobacterium tuberculosis (M. Tb). The interaction between the bacilli and the pathogen recognition receptors regulate the innate immune response to the pathogen but can also contribute to the development of the pathology. DC-SIGN is a C-type lectin which interacts with M. Tb may play an important role in human TB, which remained to be further investigated. To better understand the role of DC-SIGN in anti-mycobacterial immunity, we have used the murine model of M. Tb infection. Among the eight murine homologues (SIGNR1 to 8), SIGNR1 and SIGNR3 are the most similar homologues to DC-SIGN The infection of the mouse lines inactivated in those 2 candidates and SIGNR5 have shown that only SIGNR3-deficient mice display a higher susceptibility to the early phases of infection. Like DC-SIGN, SIGNR3 is induced in pulmonary phagocytes in infected animals. SIGNR3 can recognize glycosylated mycobacterial ligands and the whole bacteria to allow their internalization and to induce the secretion of effectors of the immune response. In vitro, we have shown that SIGNR3 signaling is dependent on a tyrosine motif and relies on the kinase SYK which activates the immune-modulatory transduction cascade. Our results suggest that SIGNR3 is the functional homologue of DC-SIGN and contributes to the protection of the host. Preliminary results suggest that DC-SIGN stimulation may also promote the secretion of pro-inflammatory cytokines in human macrophages. In summary, our results challenge the current dogma on the role of DC-SIGN as an immune escape receptor, and rather suggest that DC-SIGN may be a key-component of the defense system against M. Tb and possibly other pathogens, which remains to be evaluated in human.
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://thesesups.ups-tlse.fr/717/1/Tanne_Antoine.pdf
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

Central Library (ISO-9001:2015 Certified)
Indian Institute of Technology Kharagpur
Kharagpur, West Bengal, India | PIN - 721302

See location in the Map
03222 282435
Mail: support@ndl.gov.in

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in