What is the role of IL-22?
IL-22 is a cytokine that is important for the modulation of tissue responses during inflammation. Through activation of Stat3-signaling cascades, the cytokine induces proliferative and anti-apoptotic pathways, as well as anti-microbial molecules, that help prevent tissue damage and aid in its repair.
Is IL-22 a proinflammatory cytokine?
Although IL-22 is beneficial to the host in many infectious and inflammatory disorders, depending on the target tissue it can be pathogenic due to its inherent pro-inflammatory properties, which are further enhanced when IL-22 is released together with other pro-inflammatory cytokines, in particular IL-17.
Is IL-22 pro or anti inflammatory?
IL-22 is a pro- and anti-inflammatory cytokine that is mainly produced by T cells and NK cells. Recent studies have reported the increased number of IL-22 producing T cells in patients with autoimmune noninfectious uveitis; however, the correlation between IL-22 and uveitis remains unclear.
What interleukin activates macrophages?
Interleukin 8 (IL-8) is an α-chemokine produced by many cell types in mammals – e.g.macrophages, monocytes, epithelial cells, neutrophils and fibroblasts – upon infection or when stimulated by cytokines like IL-1β and TNF-α.
What activates Th17?
The secretion of IL-23 from antigen-presenting cells such as dendritic cells, which have been activated by the uptake and processing of pathogens, in turn activates Th17 cells.
Do Th17 cells produce IL-22?
Th17 cells are the main producers of IL-22. IL-22 is a member of the IL-10 family, along with IL-10, IL-19, IL-20, IL-24, and IL-26 (16). Activation of human CD4+ T cells with IL-12 and anti–IL-4 enhances IL-22 transcript expression, suggesting that IL-22 is a Th1 cytokine (17).
What is the function of IL-23?
IL-23 functions in innate and adaptive immunity, and is a key cytokine for promoting inflammatory responses in a variety of target organs. The most important function ascribed to IL-23 is its role in the development and differentiation of effector Th17 cells via activation of STAT3.
Which cytokine activates macrophages?
Albeit phagocytosis may provide the initial antigen stimulus, the activity of macrophages can be increased by cytokines secreted by helper T cells, with interferon gamma (IFN-γ) being one of the most potent macrophage activators.
Are macrophages involved in phagocytosis?
Macrophages work as innate immune cells through phagocytosis and sterilization of foreign substances such as bacteria, and play a central role in defending the host from infection.
What is a key action of IL 4 and IL 13?
Interleukin (IL)-4 and IL-13 are related cytokines that regulate many aspects of allergic inflammation. They play important roles in regulating the responses of lymphocytes, myeloid cells, and non-hematopoietic cells.
How is IL-4 used to inhibit phagocytosis?
Inhibition of phagocytosis extended to several other microbial particles, zymosan, and other bacteria. Concomitantly, IL-4 potentiated the secretion of proinflammatory cytokines, after additional bacterial stimulation, which depended on the MyD88 signaling pathway.
What happens to macrophages after IL-4 pretreatment?
After 8 to 12 hours of IL-4 pretreatment, the nonopsonic phagocytic uptake of N meningitidis was markedly reduced, depending on the common IL-4Ralpha chain, but independent of Scavenger receptor A and macrophage receptor with collagenous structure (MARCO), 2 known receptors for N meningitidis.
What happens to IL-12 at higher IgG density?
At slightly higher IgG densities IL-12 production is shut off and eventually IL-10 induction occurs. Thus, the myriad events emanating from FcγR ligation depends on the density of immune complexes, allowing the Fc receptors to fine-tune cellular responses depending on the extent of receptor cross-linking.
How are IgG density and macrophage Fc related?
At progressively higher densities of IgG, Fc receptor-mediated phagocytosis resulted in an inhibition of IL-12 production and then an induction of IL-10. The reciprocal alterations in these two cytokines occurred when as little as one optimally opsonized SRBC was bound per macrophage.
