알레르기비염환자 코점막 상피세포에서 IL-4, IL-13, TNF-α 자극에 의한 Thymus and Activation-Regulated Chemokine의 발현
Background:Thymus and Activation-Regulated Chemokine (TARC) is a highly specific ligand for CCR4 expressed in Th2 lymphocytes. Local production of TARC may play an important role in the induction and maintenance of allergic inflammation with the infiltration of Th2 lymphocytes. However, the cellular...
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Published in | Journal of rhinology pp. 129 - 133 |
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Main Authors | , , , |
Format | Journal Article |
Language | Korean |
Published |
대한비과학회
01.11.2008
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Subjects | |
Online Access | Get full text |
ISSN | 1229-1498 2384-4361 |
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Summary: | Background:Thymus and Activation-Regulated Chemokine (TARC) is a highly specific ligand for CCR4 expressed in
Th2 lymphocytes. Local production of TARC may play an important role in the induction and maintenance of allergic
inflammation with the infiltration of Th2 lymphocytes. However, the cellular sources of TARC among patients with allergic
rhinitis (AR) remain unclear. Objective:We investigated that nasal epithelial cells from AR could produce TARC and that
they could produce TARC differently by various stimulation of cytokines. Methods:Inferior turbinate mucosal tissues were
collected from six patients with AR sensitized to house dust mite. Nasal epithelial cells were isolated, cultured and stimulated
with IL-4, IL-13 or TNF-a alone or in combination. The level of TARC in the supernatant was measured by ELISA and mRNA
expression of that in the cells by RT-PCR. Results:The level of TARC from cultured nasal epithelial cells (CNEC) among
allergic rhinitis patients was higher than that in the control group. IL-4 or IL-13 or TNF-a alone did not upregulate TARC
production from CNEC. However, Th2 cytokines in combination with TNF-a increased the production of TARC in CNEC.
Conclusion:IL-4, IL-13 and TNF-a could upregulate TARC production from nasal epithelial cells in allergic rhinitis and
contribute to the infiltration of Th2 cells to the tissue during allergic inflammation. KCI Citation Count: 0 |
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Bibliography: | G704-002180.2008.15.2.016 |
ISSN: | 1229-1498 2384-4361 |