Premium
Cellular and molecular mechanisms involved in the resolution of innate leukocyte inflammation
Author(s) -
Rahtes Allison,
Geng Shuo,
Lee Christina,
Li Liwu
Publication year - 2018
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.3ma0218-070r
Subject(s) - inflammation , biology , innate immune system , immunology , autophagy , homeostasis , neuroscience , microbiology and biotechnology , immune system , genetics , apoptosis
Inflammation is a host response to infection or damage and is vital for clearing pathogens and host debris. When this resolution fails to occur, chronic inflammation ensues. Chronic inflammation is typically characterized as a low‐grade, persistent inflammatory process that can last for months or even years. This differs from acute inflammation, which is typically a fast, robust response to a stimulus followed by resolution with return to homeostasis. Inflammation resolution occurs through a variety of cellular processes and signaling components that act as “brakes” to keep inflammation in check. In cases of chronic inflammation, these “brakes” are often dysfunctional. Due to its prevalent association with chronic diseases, there is growing interest in characterizing these negative regulators and their cellular effects in innate leukocytes. In this review, we aim to describe key cellular and molecular homeostatic regulators of innate leukocytes, with particular attention to the emerging regulatory processes of autophagy and lysosomal fusion during inflammation resolution.