Zobrazeno 1 - 10
of 25
pro vyhledávání: '"Ellen J Lee"'
Autor:
Ellen J. Lee, Ruth J. Napier, Emily E. Vance, Sydney J. Lashley, Agnieszka D. Truax, Jenny P. Ting, Holly L. Rosenzweig
Publikováno v:
Journal of Neuroinflammation, Vol 19, Iss 1, Pp 1-12 (2022)
Abstract Background Nod-like receptors (NLRs) are critical to innate immune activation and induction of adaptive T cell responses. Yet, their role in autoinflammatory diseases of the central nervous system (CNS) remains incompletely defined. The NLR,
Externí odkaz:
https://doaj.org/article/3b4bcaf15f1940b58f3ab9e37312b029
Autor:
Ruth J. Napier, Ellen J. Lee, Michael P. Davey, Emily E. Vance, João M. Furtado, Paige E. Snow, Kimberly A. Samson, Sydney J. Lashley, Brieanna R. Brown, Reiko Horai, Mary J. Mattapallil, Biying Xu, Michelle C. Callegan, Luke S. Uebelhoer, Christina L. Lancioni, Richard K. Vehe, Bryce A. Binstadt, Justine R. Smith, Rachel R. Caspi, Holly L. Rosenzweig
Publikováno v:
Nature Communications, Vol 11, Iss 1, Pp 1-16 (2020)
How mutations in the microbial receptor NOD2 induce Blau syndrome in humans and related uveitis is unclear. Here the authors show, using Nod2-deficient mice and experimental uveitis, that Nod2 negatively regulates T cell activation and transcription
Externí odkaz:
https://doaj.org/article/5c09fe5a329b4c398f56c7642549fe79
Autor:
Ellen J. Lee, Ruth J. Napier, Emily E. Vance, Sydney J. Lashley, Agnieszka D. Truax, Jenny P. Ting, Holly L. Rosenzweig
Publikováno v:
Journal of neuroinflammation. 19(1)
Background Nod-like receptors (NLRs) are critical to innate immune activation and induction of adaptive T cell responses. Yet, their role in autoinflammatory diseases of the central nervous system (CNS) remains incompletely defined. The NLR, Nlrp12,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a957d054432f01af1c62d7235235e688
https://pubmed.ncbi.nlm.nih.gov/35313917
https://pubmed.ncbi.nlm.nih.gov/35313917
Autor:
Kylie Koney, Sydney J Lashley, Ellen J Lee, Emily E Vance, Dana J Philpott, Jae W Dugan, Michael M Davey, Holly L. Rosenzweig, Ruth J Napier
Publikováno v:
The Journal of Immunology. 208:58.08-58.08
We recently discovered a role for Nod2 within T cells in controlling Th17-immunity, such that deletion of Nod2 exacerbated experimental autoimmune arthritis and uveitis. Protection against opportunistic Candida albicans infection relies on intact Th1
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::611c9161c54233f270574e62d354411e
https://doi.org/10.4049/jimmunol.208.supp.58.08
https://doi.org/10.4049/jimmunol.208.supp.58.08
Autor:
Ruth J Napier, Emily E Vance, Kylie V Koney, Ellen J Lee, Michael M Davey, Holly L. Rosenzweig
Publikováno v:
The Journal of Immunology. 208:159.01-159.01
Children with mutations in the nucleotide binding domain of NOD2 cause the monogenetic inflammatory disease Blau Syndrome, which is characterized by dermatitis, arthritis and uveitis. NOD2 is a well-known microbial sensor important in anti-bacterial
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::5d69ccfcbf913edb4f8535ec778d90e2
https://doi.org/10.4049/jimmunol.208.supp.159.01
https://doi.org/10.4049/jimmunol.208.supp.159.01
Publikováno v:
The Journal of Immunology. 206:60.11-60.11
Caspase recruitment domain-containing protein 9 (Card9) promotes anti-fungal immunity following C-type lectin receptor Dectin-1 activation by b-glucans. CARD9 has also been implicated in the pathogenesis of T cell-mediated inflammatory diseases inclu
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::1dfcfc41ab004369f3c6c9f513627a4e
https://doi.org/10.4049/jimmunol.206.supp.60.11
https://doi.org/10.4049/jimmunol.206.supp.60.11
Autor:
Sydney J Lashley, Ellen J Lee, Emily E Vance, Jae W Dugan, Dana J Philpott, Michael P Davey, Holly L Rosenzweig, Ruth J Napier
Publikováno v:
The Journal of Immunology. 206:16.20-16.20
Nucleotide-binding oligomerization domain-containing protein 2 (Nod2) is a pattern recognition receptor known to promote anti-bacterial immunity yet its function in fungal disease is less understood. Here we sought to investigate the role of Nod2 in
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::cb9c6760a1154e0f852adfcd56de1306
https://doi.org/10.4049/jimmunol.206.supp.16.20
https://doi.org/10.4049/jimmunol.206.supp.16.20
Aberrant interleukin-1 signalling does not increase susceptibility of mice to NOD2-dependent uveitis
Publikováno v:
Clinical & Experimental Ophthalmology. 43:349-357
Background NOD2 is the genetic cause of Blau syndrome, an autoinflammatory disease that manifests as coincident uveitis and arthritis. Since dysregulation of IL-1 signalling is considered a pathogenic mechanism in a number of related autoinflammatory
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::9d3439c6817bd8f1ae8961fd1deb5079
https://doi.org/10.1111/ceo.12438
https://doi.org/10.1111/ceo.12438
Publikováno v:
Ophthalmic Research. 47:128-134
Purpose: Here we investigate the role of donor endothelium on allograft rejection in a lamellar keratoplasty (LK) model using grafts with or without donor endothelium. Methods: Corneal buttons of donor C57BL/6 mice (2.0 mm) were transplanted to lamel
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::740582032f112260b4f27187a35ec96a
https://doi.org/10.1159/000330271
https://doi.org/10.1159/000330271
Autor:
Ruth J. Napier, Ellen J. Lee, Emily E. Vance, Paige E. Snow, Clare Dawson, Peter Stenzel, Michael P. Davey, Shimon Sakaguchi, Holly L. Rosenzweig
Publikováno v:
The Journal of Immunology. 200:162.1-162.1
Nod2 is a pattern recognition receptor known for its role in antimicrobial immunity. Intriguingly, NOD2 appears to have a role outside of infection, as a single point mutation in this molecule leads to 100% incidence of an inflammatory arthritis call
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::7a2fa71c993fe58410be722d2b4c823a
https://doi.org/10.4049/jimmunol.200.supp.162.1
https://doi.org/10.4049/jimmunol.200.supp.162.1