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Absence of the cystic fibrosis transmembrane regulator ( Cftr ) from myeloid‐derived cells slows resolution of inflammation and infection
Author(s) -
Bonfield T. L.,
Hodges C. A.,
Cotton C. U.,
Drumm M. L.
Publication year - 2012
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0412188
Subject(s) - cystic fibrosis , biology , myeloid , inflammation , immunology , cystic fibrosis transmembrane conductance regulator , phenotype , myeloid cells , bone marrow , innate immune system , pseudomonas aeruginosa , immunity , lung , microbiology and biotechnology , immune system , gene , bacteria , medicine , genetics
Cftr is directly involved in myeloid cell function, contributing to the pathophysiological phenotype of the CF lung.

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