Zobrazeno 1 - 10
of 18
pro vyhledávání: '"Ravisankar A. Ramadas"'
Autor:
Cristina St Pierre, Jane Guo, John D Shin, Laura W Engstrom, Hyun-Hee Lee, Alan Herbert, Laura Surdi, James Baker, Michael Salmon, Sanjiv Shah, J Michael Ellis, Hani Houshyar, Michael A Crackower, Melanie A Kleinschek, Dallas C Jones, Alexandra Hicks, Dennis M Zaller, Stephen E Alves, Ravisankar A Ramadas
Publikováno v:
PLoS ONE, Vol 12, Iss 7, p e0180870 (2017)
While the immune system is essential for the maintenance of the homeostasis, health and survival of humans, aberrant immune responses can lead to chronic inflammatory and autoimmune disorders. Pharmacological modulation of drug targets in the immune
Externí odkaz:
https://doaj.org/article/a511e5553a1e4c19982a055d21745012
Publikováno v:
PLoS ONE, Vol 7, Iss 9, p e45784 (2012)
Interleukin (IL-) 36 cytokines (previously designated as novel IL-1 family member cytokines; IL-1F5- IL-1F10) constitute a novel cluster of cytokines structurally and functionally similar to members of the IL-1 cytokine cluster. The effects of IL-36
Externí odkaz:
https://doaj.org/article/41d7911ab2064cfd8110a49f38a926fe
Publikováno v:
Journal of Leukocyte Biology. 100:339-349
TLRs facilitate the recognition of pathogens by immune cells and the initiation of the immune response, leading to the production of proinflammatory cytokines and chemokines. Production of proinflammatory mediators by innate immune cells, such as mac
Autor:
Thomas Ludwig, James J. Moon, Ravisankar A. Ramadas, Marly I. Roche, Ramnik J. Xavier, Benjamin D. Medoff
Publikováno v:
The Journal of Immunology. 187:6197-6207
CARMA1 is a lymphocyte-specific scaffold protein necessary for T cell activation. Deletion of CARMA1 prevents the development of allergic airway inflammation in a mouse model of asthma due to a defect in naive T cell activation. However, it is unknow
Publikováno v:
American Journal of Respiratory Cell and Molecular Biology. 44:134-145
Interleukin-1 (IL-1) is a proinflammatory cytokine that signals through the Type I IL-1 receptor (IL-1RI). Novel IL-1–like cytokines were recently identified. Their functions in lung disease remain unclear. Interleukin-1 family member–9 (IL-1F9)
Publikováno v:
The Journal of Immunology. 182:1560-1567
Mice lacking surfactant protein A (SP-A) are susceptible to bacterial infection associated with an excessive inflammatory response in the lung. To determine mechanisms by which SP-A is antiinflammatory in the lung during bacterial infection, SP-A reg
Publikováno v:
DNA Sequence. 18:190-195
Asthma is a common respiratory disease that is driven by both genetic and environmental factors. Identification of the genes underlying asthma will provide insight into the mechanisms and treatment of this important disease. Previous studies in this
Autor:
Hikaru Nishio, Jacob E. Kohlmeier, Ravisankar A. Ramadas, Andrew T. Gewirtz, Asma Nusrat, Benoit Chassaing, Charles A. Parkos, Timothy L. Denning, Duke Geem, Loukia N. Lili, Jennifer E. Towne, Philipp-Alexander Neumann, Oscar Medina-Contreras, Akihito Harusato, Vu L. Ngo, Giovanna Leoni, Kyle L. Flannigan
Publikováno v:
Journal of immunology (Baltimore, Md. : 1950). 196(1)
IL-1 family members are central mediators of host defense. In this article, we show that the novel IL-1 family member IL-36γ was expressed during experimental colitis and human inflammatory bowel disease. Germ-free mice failed to induce IL-36γ in r
Autor:
Dennis M. Shubitowski, Marsha Wills-Karp, Susan Ewart, Sridhar Samineni, Ravisankar A. Ramadas, Xingnan Li
Publikováno v:
Immunogenetics. 58:851-855
Interleukin-1 receptor antagonist (IL-1ra) is an inhibitor of the proinflammatory IL-1. The IL-1ra gene (Il1rn) maps near the allergen-induced bronchial hyper-responsiveness-1 locus, Abhr1, which we previously mapped to murine chromosome 2 using A/J
Autor:
Ana Pardo-Saganta, Jayaraj Rajagopal, Khristianna Jones, Ramnik J. Xavier, Benjamin Causton, Josalyn L. Cho, Benjamin D. Medoff, Ravisankar A. Ramadas
Publikováno v:
Journal of immunology (Baltimore, Md. : 1950). 195(2)
Innate immune responses to allergens by airway epithelial cells (AECs) help initiate and propagate the adaptive immune response associated with allergic airway inflammation in asthma. Activation of the transcription factor NF-κB in AECs by allergens