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논문 기본 정보

자료유형
학술저널
저자정보
Tae-Hyoun Kim (Seoul National University) Dong-Jae Kim (Konyang University) Jae-Hak Park (Seoul National University) Jong-Hwan Park (Chonnam National University)
저널정보
대한면역학회 Immune Network Immune Network Vol.14 No.5
발행연도
2014.10
수록면
249 - 254 (6page)

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초록· 키워드

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Allergic asthma is a chronic pulmonary inflammatory disease characterized by reversible airway obstruction, hyperresponsiveness and eosinophils infiltration. Toll-like receptors (TLRs) signaling are closely associated with asthma and have emerged as a novel therapeutic target in allergic disease. The functions of TLR3 and TLR4 in allergic airway inflammation have been studied; however, the precise role of TIR-domain-containing adapter-inducing interferon-β (TRIF), the adaptor molecule for both TLR3 and TLR4, is not yet fully understood. To investigate this, we developed a mouse model of OVA-induced allergic airway inflammation and compared the severity of allergic airway inflammation in WT and TRIF?/? mice. Histopathological assessment revealed that the severity of inflammation in airway inflammation in TRIF-deficient mice was comparable to that in WT mice. The total number of cells recovered from bronchoalveolar lavage fluid did not differ between WT and TRIF-deficient mice. Moreover, TRIF deficiency did not affect Th1 and Th2 cytokine production in lung tissue nor the level of serum OVA-specific IgE, IgG<SUB>1</SUB> and IgG<SUB>2c</SUB>. These findings suggest that TRIF-mediated signaling may not be critical for the development of allergic airway inflammation.

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INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2016-511-001754608