Zobrazeno 1 - 10
of 194
pro vyhledávání: '"János G Filep"'
Autor:
János G Filep
Publikováno v:
EMBO Molecular Medicine, Vol 15, Iss 1, Pp n/a-n/a (2023)
C‐reactive protein (CRP) is a marker of acute inflammation and modulator of host defense against infections. CRP exists in conformationally distinct forms that exhibit opposing biological functions and could amplify tissue damage. Therefore, therap
Externí odkaz:
https://doaj.org/article/c29592ed01f943658d64b0ede9f43928
Publikováno v:
PLoS ONE, Vol 9, Iss 1, p e87006 (2014)
Neutrophils detect bacterial constituents, including bacterial DNA (CpG DNA), which elicits innate immunity and prolongs the functional life span of neutrophils through suppression of apoptosis. Both the anti-apoptotic protein Mcl-1 and activation of
Externí odkaz:
https://doaj.org/article/dad0379a9c9d4fa182f70c5465ac9724
Autor:
János G. Filep
Publikováno v:
Journal of Clinical Investigation. 133
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::d8688b8e1448d33ea0fc892345d21def
https://doi.org/10.1172/jci170643
https://doi.org/10.1172/jci170643
Publikováno v:
Frontiers in Immunology. 13
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::39c29b3e15e6a6258e911e49600f41f1
https://doi.org/10.3389/fimmu.2022.1103379
https://doi.org/10.3389/fimmu.2022.1103379
Publikováno v:
Proceedings of the National Academy of Sciences of the United States of America. 119(31)
Aberrant immune responses, including hyperresponsiveness to Toll-like receptor (TLR) ligands, underlie acute respiratory distress syndrome (ARDS). Type I interferons confer antiviral activities and could also regulate the inflammatory response, where
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::009d66ff6a36e0ad07d937d598216c83
https://pubmed.ncbi.nlm.nih.gov/35878041
https://pubmed.ncbi.nlm.nih.gov/35878041
Publikováno v:
Frontiers in Immunology. 13
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9e52a1e60e1d11fb988a6bcf1d8ccc7c
Autor:
Amiram Ariel, János G. Filep
Publikováno v:
Am J Physiol Cell Physiol
Neutrophils are polymorphonuclear leukocytes that play a central role in host defense against infection and tissue injury. They are rapidly recruited to the inflamed site and execute a variety of functions to clear invading pathogens and damaged cell
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8d67a978f4ceebac7dc57bc473cde644
https://doi.org/10.1152/ajpcell.00181.2020
https://doi.org/10.1152/ajpcell.00181.2020
Publikováno v:
Proceedings of the National Academy of Sciences. 117:7971-7980
Timely resolution of bacterial infections critically depends on phagocytosis of invading pathogens by polymorphonuclear neutrophil granulocytes (PMNs), followed by PMN apoptosis and efferocytosis. Here we report that bacterial DNA (CpG DNA) and mitoc
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::7e56523ab7eb10f903967f9305c18a25
https://doi.org/10.1073/pnas.1920193117
https://doi.org/10.1073/pnas.1920193117
Autor:
János G. Filep
Publikováno v:
Frontiers in immunology. 13
Acute inflammation is a localized and self-limited innate host-defense mechanism against invading pathogens and tissue injury. Neutrophils, the most abundant immune cells in humans, play pivotal roles in host defense by eradicating invading pathogens
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a45d49538b9a90e78c8af4e5cdd779ec
https://pubmed.ncbi.nlm.nih.gov/35371088
https://pubmed.ncbi.nlm.nih.gov/35371088
Publikováno v:
Frontiers in immunology. 13
The resolution of inflammation is a temporally and spatially coordinated process that in its innate manifestations, primarily involves neutrophils and macrophages. The shutdown of infection or injury-induced acute inflammation requires termination of
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a1395a8ca546d2275aea80457853e2af
https://pubmed.ncbi.nlm.nih.gov/35615359
https://pubmed.ncbi.nlm.nih.gov/35615359