생화학분자생물학회

	Name: Yoe-Sik Bae ( yoesik@skku.edu )
	2010-present	Associate/Full Professor, Department of Biological Sciences, Sungkyunkwan University
	2008-2009	Visiting Associate Professor, Department of Pathology, Stanford University School of Medicine, USA
	2002-2010	Full time Instructor, Assistant/Associate Professor, Department of Biochemistry, Dong-A University College of Medicine
	2000-2002	Postdoctoral research fellow, POSTECH
	1998-2000	Ph.D., Department of Life Science, POSTECH

Emerging roles of neutrophils in immune homeostasis

Neutrophils, the most abundant innate immune cells, play essential roles in the innate immune system. As key innate immune cells, neutrophils detect intrusion of pathogens and initiate immune cascades with their functions; swarming (arresting), cytokine production, degranulation, phagocytosis, and projection of neutrophil extracellular trap. Because of their short lifespan and consumption during immune response, neutrophils need to be generated consistently, and generation of newborn neutrophils (granulopoiesis) should fulfill the environmental/systemic demands for training in cases of infection. Accumulating evidence suggests that neutrophils also play important roles in the regulation of adaptive immunity. Neutrophil-mediated immune responses end with apoptosis of the cells, and proper phagocytosis of the apoptotic body (efferocytosis) is crucial for initial and post resolution by producing tolerogenic innate/adaptive immune cells. However, inflammatory cues can impair these cascades, resulting in systemic immune activation; necrotic/pyroptotic neutrophil bodies can aggravate the excessive inflammation, increasing inflammatory macrophage and dendritic cell activation and subsequent TH1/TH17 responses contributing to the regulation of the pathogenesis of autoimmune disease. In this review, we briefly introduce recent studies of neutrophil function as players of immune response.


BMB Rep. 2022 Oct;55(10):473-480. DOI: 10.5483/BMBRep.2022.55.10.115.​

https://pubmed.ncbi.nlm.nih.gov/36104260/