Cutting Edge: Limiting MHC Class II Expression to Dendritic Cells Alters the Ability to Develop Th2- Dependent Allergic Airway Inflammation
Author(s) -
Naiqian Niu,
Terri M. Laufer,
Robert Homer,
Lauren Cohn
Publication year - 2009
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.0901349
Subject(s) - cd11c , immunology , mhc class ii , priming (agriculture) , inflammation , dendritic cell , immune system , allergic inflammation , mhc class i , medicine , t cell , biology , cd8 , phenotype , biochemistry , botany , germination , gene
In allergic airway inflammation, dendritic cells (DCs) are required for Th2 generation, recruitment, and activation in the respiratory tract. DCs have been shown to be necessary and sufficient for the induction of Th1 immune responses. In Th2 immunity and allergic airway inflammation, the ability of a DC to function as the sole APC has not been tested. We show that CD11c/A(beta)(b) mice with MHC class II expression restricted to CD11c-expressing DCs develop airway neutrophilia rather than allergic airway inflammation. Although CD11c/A(beta)(b) mice are capable of Th2 recruitment and activation in the lung, Th2 priming in CD11c/A(beta)(b) mice results in IFN-gamma production. Effective Th2 generation and allergic airway inflammation was achieved in CD11c/A(beta)(b) mice after treatment with anti-IFN-gamma. These studies show that DCs alone cannot drive the development of Th2 cells but require an additional MHC class II signal to stimulate effective Th2 immunity.
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