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- W2757378082 abstract "RelB is a member of the NF-κB family, which is essential for dendritic cell (DC) function and maturation. However, the contribution of RelB to the development of allergic airway inflammation (AAI) is unknown. Here, we identify a pivotal role for RelB in the development of spontaneous AAI that is independent of exogenous allergen exposure. We assessed AAI in two strains of RelB-deficient (RelB−/−) mice: one with a targeted deletion and one expressing a major histocompatibility complex transgene. To determine the importance of RelB in DCs, RelB-sufficient DCs (RelB+/+ or RelB−/−) were adoptively transferred into RelB−/− mice. Both strains had increased pulmonary inflammation compared with their respective wild-type (RelB+/+) and heterozygous (RelB+/−) controls. RelB−/− mice also had increased inflammatory cell influx into the airways, levels of chemokines (CCL2/3/4/5/11/17 and CXCL9/10/13) and T-helper cell type 2–associated cytokines (IL-4/5) in lung tissues, serum IgE, and airway remodeling (mucus-secreting cell numbers, collagen deposition, and epithelial thickening). Transfer of RelB+/− CD11c+ DCs into RelB−/− mice decreased pulmonary inflammation, with reductions in lung chemokines, T-helper cell type 2–associated cytokines (IL-4/5/13/25/33 and thymic stromal lymphopoietin), serum IgE, type 2 innate lymphoid cells, myeloid DCs, γδ T cells, lung Vβ13+ T cells, mucus-secreting cells, airway collagen deposition, and epithelial thickening. These data indicate that RelB deficiency may be a key pathway underlying AAI, and that DC-encoded RelB is sufficient to restore control of this inflammation." @default.
- W2757378082 created "2017-10-06" @default.
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- W2757378082 date "2018-03-01" @default.
- W2757378082 modified "2023-10-08" @default.
- W2757378082 title "RelB-Deficient Dendritic Cells Promote the Development of Spontaneous Allergic Airway Inflammation" @default.
- W2757378082 cites W1502985829 @default.
- W2757378082 cites W1579720523 @default.
- W2757378082 cites W1588586944 @default.
- W2757378082 cites W1615175231 @default.
- W2757378082 cites W1634158134 @default.
- W2757378082 cites W1637364976 @default.
- W2757378082 cites W1833894873 @default.
- W2757378082 cites W1840215279 @default.
- W2757378082 cites W1895680870 @default.
- W2757378082 cites W1896531240 @default.
- W2757378082 cites W1966365711 @default.
- W2757378082 cites W1967376415 @default.
- W2757378082 cites W1975696541 @default.
- W2757378082 cites W1978214088 @default.
- W2757378082 cites W1984387148 @default.
- W2757378082 cites W1994017311 @default.
- W2757378082 cites W1997055154 @default.
- W2757378082 cites W1997512963 @default.
- W2757378082 cites W2009545748 @default.
- W2757378082 cites W2009993815 @default.
- W2757378082 cites W2014859732 @default.
- W2757378082 cites W2018245598 @default.
- W2757378082 cites W2018718597 @default.
- W2757378082 cites W2020759184 @default.
- W2757378082 cites W2022928437 @default.
- W2757378082 cites W2033810895 @default.
- W2757378082 cites W2035165308 @default.
- W2757378082 cites W2035499658 @default.
- W2757378082 cites W2036841570 @default.
- W2757378082 cites W2037291153 @default.
- W2757378082 cites W2047715167 @default.
- W2757378082 cites W2056734272 @default.
- W2757378082 cites W2058266230 @default.
- W2757378082 cites W2058310513 @default.
- W2757378082 cites W2059190502 @default.
- W2757378082 cites W2068144837 @default.
- W2757378082 cites W2068870295 @default.
- W2757378082 cites W2069759825 @default.
- W2757378082 cites W2073290862 @default.
- W2757378082 cites W2076980233 @default.
- W2757378082 cites W2078303207 @default.
- W2757378082 cites W2085592918 @default.
- W2757378082 cites W2094294562 @default.
- W2757378082 cites W2094452595 @default.
- W2757378082 cites W2094863064 @default.
- W2757378082 cites W2096572691 @default.
- W2757378082 cites W2098778820 @default.
- W2757378082 cites W2098912300 @default.
- W2757378082 cites W2100630603 @default.
- W2757378082 cites W2103585613 @default.
- W2757378082 cites W2103842702 @default.
- W2757378082 cites W2106790228 @default.
- W2757378082 cites W2108622955 @default.
- W2757378082 cites W2122044177 @default.
- W2757378082 cites W2124871836 @default.
- W2757378082 cites W2127236650 @default.
- W2757378082 cites W2127413321 @default.
- W2757378082 cites W2135790224 @default.
- W2757378082 cites W2138049964 @default.
- W2757378082 cites W2140052458 @default.
- W2757378082 cites W2140686309 @default.
- W2757378082 cites W2141475970 @default.
- W2757378082 cites W2151288926 @default.
- W2757378082 cites W2154110743 @default.
- W2757378082 cites W2157710399 @default.
- W2757378082 cites W2158507525 @default.
- W2757378082 cites W2161167143 @default.
- W2757378082 cites W2214249404 @default.
- W2757378082 cites W2243398804 @default.
- W2757378082 cites W2342508582 @default.
- W2757378082 cites W2439973029 @default.
- W2757378082 cites W2710187462 @default.
- W2757378082 cites W4294250611 @default.
- W2757378082 cites W4313347838 @default.
- W2757378082 cites W4319308391 @default.
- W2757378082 doi "https://doi.org/10.1165/rcmb.2017-0242oc" @default.
- W2757378082 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28960101" @default.
- W2757378082 hasPublicationYear "2018" @default.
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