Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Mark Wewers"'
Autor:
Anwari Akhter, Angélica Olmo-Fontánez, Juan Moliva, Abul Azad, Holden Kelley, Julia Scordo, Mikhail Gavrilin, Mark Wewers, Jordi Torrelles
Publikováno v:
The Journal of Immunology. 202:62.20-62.20
Tuberculosis (TB) is the leading killer of people with HIV infection. Limited studies have considered HIV infection associated changes to the soluble components of the innate immune system in the alveolar lining fluid (ALF) as a contributing factor t
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::a60546da97bd3b2d095774f36863ec79
https://doi.org/10.4049/jimmunol.202.supp.62.20
https://doi.org/10.4049/jimmunol.202.supp.62.20
Autor:
Fabien Habyarimana, Nina Napolitano, Christian C. McAndrew, Srabani Mitra, Anasuya Sarkar, Mikhail A. Gavrilin, Mark Wewers
Publikováno v:
The Journal of Immunology. 200:115.3-115.3
Background Pyrin is a member of the TRIM family of proteins. Pyrin senses RhoA posttranslational modifications that inactivate RhoA, resulting in the formation of a pyrin inflammasome. Clostridium difficile TcdB toxin inactivates RhoA by glycation of
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::4f23dbdabbeb2aa591b8b50fe08ee5ca
https://doi.org/10.4049/jimmunol.200.supp.115.3
https://doi.org/10.4049/jimmunol.200.supp.115.3
Autor:
Kruthika Sundaram, Mark Wewers
Publikováno v:
The Journal of Immunology. 194:53.11-53.11
Rationale: Asthma is a chronic lung disease characterized by inflammation of bronchial epithelium. House dust mite (HDM) is a common allergen that triggers asthma. IκBζ is a newly recognized member of the NFκB family that is induced in lung epithe
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::6aab99ff822ebfcd793b01cd30737b7c
https://doi.org/10.4049/jimmunol.194.supp.53.11
https://doi.org/10.4049/jimmunol.194.supp.53.11
Publikováno v:
The Journal of Immunology. 192:128.14-128.14
Lung epithelial cell death is critical to acute lung injury. It is known that FasL plays a prominent role in lung cell death and may work in part through activation of the receptor interacting protein-2 (RIP2). RIP2 is serine/threonine kinase with a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::f3bbed55eeeb6c0b0e857c602c49f514
https://doi.org/10.4049/jimmunol.192.supp.128.14
https://doi.org/10.4049/jimmunol.192.supp.128.14
Publikováno v:
The Journal of Immunology. 192:57.4-57.4
Caspase-1 is an inflammatory protease which is required for activation of the pro-inflammatory cytokines, interleukin-1β (IL-1β) and IL-18, in addition to a role in a form of cell death termed pyroptosis. Caspase-1 is synthesized as a zymogen which
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::5e72f6970ce8e3a3734779ac83fa434c
https://doi.org/10.4049/jimmunol.192.supp.57.4
https://doi.org/10.4049/jimmunol.192.supp.57.4
Publikováno v:
The Journal of Immunology. 192:62.6-62.6
Inflammasomes play key roles in the innate immune response to pathogens and tissue injury. Inflammasome assembly involves two distinct steps; priming and activation, which together trigger caspase-1 to process and release IL-1β, IL-18 and in some se
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::626b8e60c622a0269cc7cb2465770f51
https://doi.org/10.4049/jimmunol.192.supp.62.6
https://doi.org/10.4049/jimmunol.192.supp.62.6
Publikováno v:
The Journal of Immunology. 178:S182-S183
IFNγ and caspase-1 have a reciprocal relationship. INFγ induces caspase-1 expression but caspase-1 is critical to the activation of the INFγ inducing factor IL-18. To investigate the INFγ inducing function of caspase-1 we characterized the INFγ
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::e82fe6b588beb59da4fd0f83f10d3b68
https://doi.org/10.4049/jimmunol.178.supp.95.30
https://doi.org/10.4049/jimmunol.178.supp.95.30
Autor:
Devyn Gillette, Prexy Shah, Thomas Cremer, Mikhail Gavrilin, Beth Besecker, Anasuya Sarkar, Daren Knoell, Estelle Cormet-Boyaka, Mark Wewers, Jonathan Butchar, Susheela Tridandapani
Publikováno v:
The Journal of Immunology. 190:56.15-56.15
Burkholderia cenocepacia is the causative agent of the fatal lung disease, Cepacia syndrome. Epithelial cells are the first cells challenged in airway infections, yet, their pro-inflammatory response to B. cenocepacia remains under investigated. Here
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::e6ad3e61616ee79abf7248ae84390980
https://doi.org/10.4049/jimmunol.190.supp.56.15
https://doi.org/10.4049/jimmunol.190.supp.56.15
Autor:
Marco Cardone, Amiran Dzutsev, Hongchuan Li, Franca Gerosa, Robin Winkler-Pickett, Lisa Provezza, Elena Riboldi, Selinda Orr, Folkert Steinhagen, Mark Wewers, Daniel McVicar, Stephen Anderson, Romina Goldszmid, Lyudmila Lyakh, Giorgio Trinchieri
Publikováno v:
The Journal of Immunology. 190:193.9-193.9
The molecular networks controlling the DC programming in response to C-type lectin receptor agonists including beta-glucan, a fungal and bacterial component and ligand for the Dectin-1 receptor, are still poorly characterized. We studied these immuno
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::efd9679e3025ae2e680b0ba011043aa8
https://doi.org/10.4049/jimmunol.190.supp.193.9
https://doi.org/10.4049/jimmunol.190.supp.193.9
Autor:
Mingjie Liu, Shengying Bao, Marina Gálvez-Peralta, Charlie Pyle, Andrew Rudawsky, Daniel Nebert, Mark Wewers, Daren Knoell
Publikováno v:
The Journal of Immunology. 186:116.33-116.33
Zinc is an essential micronutrient required for proper immune function. We previously reported that zinc deficiency increases inflammation and mortality in response to polymicrobial sepsis. Here we report that a specific zinc transporter, SLC39A8 (ZI
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::cdc3ea277fa9fb3f34f578463de99956
https://doi.org/10.4049/jimmunol.186.supp.116.33
https://doi.org/10.4049/jimmunol.186.supp.116.33