RT info:eu-repo/semantics/article
T1 Fas-activated serine/threonine phosphoprotein promotes immune-mediated pulmonary inflammation
A1 Simarro Grande, María
A1 Giannattasio, Giorgio
A1 Fuente García, Miguel Ángel de la
A1 Benarafa, Charaf
A1 Subramanian, Kulandayan K.
A1 Ishizawar, Rumey
A1 Balestrieri, Barbara
A1 Andersson, Emma M.
A1 Luo, Hongbo R.
A1 Orduña Domingo, Antonio
A1 Boyce, Joshua
K1 Sistema inmunitario-Enfermedades
AB We generated Fas-activated serine threonine phosphoprotein (FAST)-deficient mice (FAST−/−) to study the in vivo role of FAST in immune system function. In a model of house dust mite-induced allergic pulmonary inflammation, wild type mice develop a mixed cellular infiltrate composed of eosinophils, lymphocytes, and neutrophils. FAST−/− mice develop airway inflammation that is distinguished by the near absence of neutrophils. Similarly, LPS-induced alveolar neutrophil recruitment is markedly reduced in FAST−/− mice compared with wild type controls. This is accompanied by reduced concentrations of cytokines (TNF-α and IL-6 and -23) and chemoattractants (MIP-2 and keratinocyte chemoattractant) in bronchoalveolar lavage fluids. Because FAST−/− neutrophils exhibit normal chemotaxis and survival, impaired neutrophil recruitment is likely to be due to reduced production of chemoattractants within the pulmonary parenchyma. Studies using bone marrow chimeras implicate lung resident hematopoietic cells (e.g., pulmonary dendritic cells and/or alveolar macrophages) in this process. In conclusion, our results introduce FAST as a proinflammatory factor that modulates the function of lung resident hematopoietic cells to promote neutrophil recruitment and pulmonary inflammation.
PB American Association of Immunologists
SN 0022-1767
YR 2010
FD 2010
LK http://uvadoc.uva.es/handle/10324/9817
UL http://uvadoc.uva.es/handle/10324/9817
LA eng
NO J Immunol. 2010; 184(9): 5325–5332.
NO Producción Científica
DS UVaDOC
RD 22-nov-2024