Počet záznamů: 1
The Tick Protein Sialostatin L2 Binds to Annexin A2 and Inhibits NLRC4-Mediated Inflammasome Activation
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SYSNO ASEP 0463420 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název The Tick Protein Sialostatin L2 Binds to Annexin A2 and Inhibits NLRC4-Mediated Inflammasome Activation Tvůrce(i) Wang, X. (US)
Shaw, D.K. (US)
Sakhon, O. S. (US)
Snyder, G.A. (US)
Sundberg, E.J. (US)
Santambrogio, L. (US)
Sutterwala, F.S. (US)
Dumlera, J.S. (US)
Shirey, K.A. (US)
Perkins, D.J. (US)
Richard, K. (US)
Chagas, A. C. (US)
Calvo, E. (US)
Kopecký, J. (CZ)
Kotsyfakis, Michalis (BC-A) RID, ORCID
Pedra, J. H. F. (US)Zdroj.dok. Infection and Immunity. - : American Society for Microbiology - ISSN 0019-9567
Roč. 84, č. 6 (2016), s. 1796-1805Poč.str. 10 s. Forma vydání Tištěná - P Jazyk dok. eng - angličtina Země vyd. US - Spojené státy americké Klíč. slova Anaplasma phagocytophilum ; bacterial ligands ; NAIP/NLRC4 inflammasomes Vědní obor RIV EC - Imunologie Institucionální podpora BC-A - RVO:60077344 UT WOS 000377106900013 EID SCOPUS 84971505816 DOI 10.1128/IAI.01526-15 Anotace Tick saliva contains a number of effector molecules that inhibit host immunity and facilitate pathogen transmission. How tick proteins regulate immune signaling, however, is incompletely understood. Here, we describe that loop 2 of sialostatin L2, an anti-inflammatory tick protein, binds to annexin A2 and impairs the formation of the NLRC4 inflammasome during infection with the rickettsial agent Anaplasma phagocytophilum. Macrophages deficient in annexin A2 secreted significantly smaller amounts of interleukin-1 beta (IL-1 beta) and IL-18 and had a defect in NLRC4 inflammasome oligomerization and caspase-1 activation. Accordingly, Annexin a2-deficient mice were more susceptible to A. phagocytophilum infection and showed splenomegaly, thrombocytopenia, and monocytopenia. Providing translational support to our findings, better binding of annexin A2 to sialostatin L2 in sera from 21 out of 23 infected patients than in sera from control individuals was also demonstrated. Overall, we establish a unique mode of inflammasome evasion by a pathogen, centered on a blood-feeding arthropod. Pracoviště Biologické centrum (od r. 2006) Kontakt Dana Hypšová, eje@eje.cz, Tel.: 387 775 214 Rok sběru 2017
Počet záznamů: 1