B Cells Produce the Tissue-Protective Protein RELMα during Helminth Infection, which Inhibits IL-17 Expression and Limits Emphysema.
Cell Rep
; 25(10): 2775-2783.e3, 2018 12 04.
Article
em En
| MEDLINE
| ID: mdl-30517865
ABSTRACT
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.
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Linfócitos B
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Infecções por Strongylida
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Interleucina-17
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Peptídeos e Proteínas de Sinalização Intercelular
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Enfisema
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Nippostrongylus
Limite:
Animals
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article