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Emphysema results in destruction of alveolar walls and enlargement of lung airspaces and has been shown to develop during helminth infections through IL-4R-independent mechanisms. We examined whether interleukin 17A (IL-17A) may instead modulate development of emphysematous pathology in mice infected with the helminth parasite Nippostrongylus brasiliensis. We found that transient elevations in IL-17A shortly after helminth infection triggered subsequent emphysema that destroyed alveolar structures. Furthermore, lung B cells, activated through IL-4R signaling, inhibited early onset of emphysematous pathology. IL-10 and other regulatory cytokines typically associated with B regulatory cell function did not play a major role in this response. Instead, at early stages of the response, B cells produced high levels of the tissue-protective protein, Resistin-like molecule α (RELMα), which then downregulated IL-17A expression. These studies show that transient elevations in IL-17A trigger emphysema and reveal a helminth-induced immune regulatory mechanism that controls IL-17A and the severity of emphysema.
Pubmed ID: 30517865 RIS Download
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laboratory mouse with name BALB/cAnNCrl from MGI.
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View all literature mentionsMus musculus with name BALB/c-Il4ratm1Sz/J from IMSR.
View all literature mentionsMus musculus with name BALB/cJ from IMSR.
View all literature mentionsThis isotype control targets Trinitrophenol
View all literature mentionsThis monoclonal targets Mouse IL-17
View all literature mentionsThis polyclonal targets Rabbit RELMa FITC
View all literature mentionsThis monoclonal targets CD138
View all literature mentionsThis monoclonal targets CD1d
View all literature mentionsThis monoclonal targets CD5
View all literature mentionsThis monoclonal targets CD24
View all literature mentionsThis monoclonal targets CD23
View all literature mentionsThis monoclonal targets CD21
View all literature mentionsThis monoclonal targets CD45R
View all literature mentionsThis monoclonal targets F4/80
View all literature mentionsThis monoclonal targets Siglec-F
View all literature mentionsThis monoclonal targets CD11b (Mac-1)
View all literature mentionsThis monoclonal targets MHC Class II I-Ab
View all literature mentionsThis monoclonal targets Ly-6G
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