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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2021.9
- 수록면
- 89 - 102 (14page)
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The ongoing coronavirus disease-2019 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus-2. COVID-19 severity is related to the cytokine storm phenomenon, which is amplified by pro-inflammatory cytokines and chemokines; it may cause extensive pulmonary damage. Among these cytokines, interleukin (IL)-17, produced mainly by T helper 17 (Th17) cells, is responsible for the immunopathological responses present in acute respiratory distress syndrome. This review discusses the roles of IL-17 and Th17 responses in the pathophysiology of COVID-19. Dysregulated Th17-responses, linked to various risk factors, may contribute to pathological inflammation through the amplification of multiple inflammatory cytokines and chemokines, as well as augmentation of neutrophil infiltration in the lungs of severe COVID-19 patients. A more detailed understanding of the roles of Th17 responses, as well as the mechanisms underlying altered IL-17 production and signaling, may improve therapeutic strategies for severe or critically ill COVID-19 patients by targeting the IL-17 pathway.
목차
INTRODUCTION
OVERVIEW OF IL-17 AND ITS SIGNALING NETWORK
ROLE OF IL-17 IN COVID-19
CONCLUSION
REFERENCES
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UCI(KEPA) : I410-ECN-0101-2021-475-002143196