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Counter regulation of the high affinity IgE receptor, FcεRI, on human airway dendritic cells by IL‐4 and IL‐10
Author(s) -
Faith A.,
Singh N.,
Chevretton E.,
Roberts D.,
Lee T.,
Corrigan C.,
Hawrylowicz C.
Publication year - 2009
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2009.02060.x
Subject(s) - immunology , cytokine , immunoglobulin e , respiratory tract , dendritic cell , medicine , receptor , flow cytometry , immune system , respiratory system , antibody
Background: Immunoglobulin E is a signalling molecule within the environment of the respiratory tract, the high affinity receptor for which, FcεRI, is expressed by dendritic cells (DC). Little is known, however, of the expression and function of FcεRI on DC in the human respiratory tract. Methods: CD1c + DC were purified from surgically resected nasal turbinates of 11 atopic and 12 nonatopic patients with chronic rhinosinusitis. Expression of FcεRI was determined by flow cytometry. Cytokine production by DC was determined by cytometric bead array. Results: Expression of FcεRI was significantly elevated on respiratory tract dendritic cells (RTDC) from atopic as compared to nonatopic patients. Activation of RTDC through FcεRI induced production of the pro‐inflammatory cytokines IL‐6 and TNF‐α, and the anti‐inflammatory cytokine IL‐10. The production of IL‐6 and TNF‐α was elevated in atopic compared to nonatopic patients studied. Conversely IL‐10 production was elevated in nonatopic patients. Concomitant activation of FcεRI and stimulation of RTDC with IL‐4 inhibited production of IL‐10 by RTDC. Neutralization experiments with anti‐IL‐10 Ab enhanced whereas addition of exogenous IL‐10 to RTDC inhibited FcεRI‐mediated inflammatory cytokine production. Conclusion: The function of FcεRI on RTDC from patients with rhinosinusitis is susceptible to counter regulation by IL‐4 and IL‐10.