Innate-adaptive immunity interplay and redox regulation in immune response

Abstract

Innate and adaptive immune cell activation and infiltration is the key characteristic of tissue inflammation. The innate immune system is the front line of host defense in which innate immune cells are activated by danger signals, including pathogen- and danger-associated molecular pattern, and metabolite-associated danger signal. Innate immunity activation can directly contribute to tissue inflammation or immune resolution by phagocytosis and secretion of biologically active molecules, or indirectly via antigen-presenting cell (APC) activation-mediated adaptive immune responses. This review article describes the cellular and molecular interplay of innate-adaptive immune systems. Three major mechanisms are emphasized in this article for their role in facilitating innate-adaptive immunity interplay. 1) APC can be formed from classical and conditional innate immune cells to bridge innate-adaptive immune response. 2) Immune checkpoint molecular pairs connect innate and adaptive immune cells to direct one-way and two-way immune checkpoint reactions. 3) Metabolic reprogramming during immune responses leads to excessive cytosolic and mitochondrial reactive oxygen species (ROS) production. Increased NADPH oxidase-derived extracellular and intracellular ROS are mostly responsible for oxidative stress, which contributes to functional changes in immune cells. Further understanding of innate-adaptive immunity interplay and its underlying molecular basis would lead to the identification of therapeutic targets for immunological and inflammatory disease.

Protective Effects of Kirenol against Lipopolysaccharide-Induced Acute Lung Injury through the Modulation of the Proinflammatory NFκB Pathway and the AMPK2-/Nrf2-Mediated HO-1/AOE Pathway

“…ROS generation is mediated by leukocytes as a defensive response to pathogen invasion [ 36 ]. ROS, in appropriate numbers, are necessary for the elimination of pathogens from the body.…”

“…ROS, in appropriate numbers, are necessary for the elimination of pathogens from the body. However, the lipid peroxidation caused by the overproduction of ROS is associated with various diseases and tissue damage [ 36 ]. ROS and relative oxidative stress constitute vital upstream components of NF-κB activation [ 19 , 37 ].…”

Redox Homeostasis in Poultry: Regulatory Roles of NF-κB

“…Redox biology is a very quickly developing area of modern biological sciences, and roles of redox homeostasis in health and disease have recently received tremendous attention [ 1 , 2 , 3 , 4 , 5 , 6 ]. There are a range of redox pairs in cells/tissues responsible for redox homeostasis maintenance/regulation.…”

Effect of Selenium and Peroxynitrite on Immune Function of Immature Dendritic Cells in Humans

“…For example, investigations in mice have reported that ROS activates DCs and promotes interaction between DCs and T cells during antigen presentation [ 4 ], as well as induces apoptosis or necrosis of DCs via Acinetobacter baumannii outer membrane protein A [ 5 ]. Among humans, ROS stimulates differentiation of mononuclear cells into DCs [ 6 ], and O 2 − assists in the maturation of imDCs into mDCs [ 7 ]. Importantly, the reaction product of O 2 − and nitric oxide (peroxynitrite) is required for cytokine production in human monocytes [ 8 ], as nitric oxide synthase inhibitors have been linked to a reduction in peroxynitrite formation and partial inhibition of O 2 − induced maturation of DCs [ 7 ].…”

“…Among humans, ROS stimulates differentiation of mononuclear cells into DCs [ 6 ], and O 2 − assists in the maturation of imDCs into mDCs [ 7 ]. Importantly, the reaction product of O 2 − and nitric oxide (peroxynitrite) is required for cytokine production in human monocytes [ 8 ], as nitric oxide synthase inhibitors have been linked to a reduction in peroxynitrite formation and partial inhibition of O 2 − induced maturation of DCs [ 7 ]. Previous studies showed that a high concentration of nitrite was found in LPS-activated mouse DCs [ 9 ]; however, the effect of nitrite in the tumor microenvironment [ 10 ] on DCs function remains unknown.…”