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Primarily, intestinal macrophages do not induce inflammatory responses. Whereas tissue macrophages release various inflammatory cytokines, such as IL-1, IL-6 and TNF-α, intestinal macrophages do not produce or secrete inflammatory cytokines. This change is directly caused by the intestinal macrophages environment.
Some inflammatory cytokines have additional roles such as acting as growth factors. [5] Pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α also trigger pathological pain. [1] While IL-1β is released by monocytes and macrophages, it is also present in nociceptive DRG neurons. IL-6 plays a role in neuronal reaction to an injury.
Cytokines are produced by a broad range of cells, including immune cells like macrophages, B lymphocytes, T lymphocytes and mast cells, as well as endothelial cells, fibroblasts, and various stromal cells; a given cytokine may be produced by more than one type of cell.
MIP-1γ is another macrophage inflammatory protein and according to the new nomenclature is named CCL9. [3] It is produced mainly by follicle-associated epithelial cells and is responsible for chemotaxis of dendritic cells and macrophages into Peyer's patches in gut through binding of CCR1. [11] MIP-1δ or MIP-5 (CCL15) binds also CCR1 and CCR3 ...
Interleukin 3 (IL3) is a cytokine that regulates hematopoiesis by controlling the production, differentiation and function of granulocytes and macrophages. [ 15 ] [ 16 ] The protein, which exists in vivo as a monomer, is produced in activated T cells and mast cells, [ 15 ] [ 16 ] and is activated by the cleavage of an N-terminal signal sequence.
Type 4 hypersensitivity, also known as delayed type hypersensitivity, are caused via the over-stimulation of immune cells, commonly lymphocytes and macrophages, resulting in chronic inflammation and cytokine release. Antibodies do not play a direct role in this allergy type.
Microglia and macrophages together help in the oligodendrocyte remyelination. [7] Intestinal injury of the epithelia activates macrophages that secrete a wide range of survival and growth progenitor factors which is very similar to muscle regeneration. M1 macrophages induce proliferative environment by secreting cytokines IL6, TNF, IL1, and G ...
When under physical stress, the release of CCL2 (cytokine) in the hair follicle induces the infiltration of macrophages. The infiltrated macrophages mainly express an M1 phenotype, which are pro-inflammatory macrophages that could trigger apoptosis of cells in the follicle by their upregulation of pro-inflammatory cytokines such as TNF-a. [2]