Systemic inflammation

From Wikipedia, the free encyclopedia
Jump to: navigation, search

Chronic systemic inflammation (SI) is the result of release of pro-inflammatory cytokines from immune-related cells and the chronic activation of the innate immune system.

It can contribute to the development or progression of certain conditions.[1]

Mechanisms Inducing SI[edit]

Release of pro-inflammatory cytokines and activation of the innate immune system may be the result of either external (biological or chemical agents) or internal (genetic mutations/variations) factors.

Lack of Control by Tolerogenic Dendritic Cells and T-regulatory Cells[edit]

While SI may be induced by multiple external factors, research suggests that a lack of control by tolerogenic dendritic cells and T-regulatory cells (Treg) is possibly the primary risk factor for the development of SI. In functioning immune responses, T-helper and T-cytotoxic cells are activated by presentation of antigens by antigen-presenting cells (APCs). Chief among these are dendritic cells (DCs). When a DC presents an antigen to a Treg cell, a signal is then sent to the nucleus of the DC, resulting in the production of Indoleamine 2,3- Dioxygenase (IDO). IDO inhibits T cell responses by depleting tryptophan and producing kynurenine, which is toxic to the cell.

Individuals susceptible to developing chronic systemic inflammation appear to lack proper functioning of Treg cells and TDCs. In these individuals, a lack of control of inflammatory processes results in multiple chemical and food intolerances, autoimmune diseases and many other symptoms and diseases.

See also[edit]

References[edit]

  1. ^ Sattar N, McCarey DW, Capell H, McInnes IB (December 2003). "Explaining how "high-grade" systemic inflammation accelerates vascular risk in rheumatoid arthritis". Circulation 108 (24): 2957–63. doi:10.1161/01.CIR.0000099844.31524.05. PMID 14676136.