Pro-Inflammatory Cytokine Response is the fundamental immunological cascade characterized by the rapid secretion of a specific class of signaling proteins, such as Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNF-α), and Interleukin-1 beta (IL-1β), by immune and non-immune cells. While essential for initiating acute, protective inflammation in response to injury or infection, a sustained or disproportionate response becomes a primary driver of chronic systemic inflammation and metabolic dysfunction.
Origin
This terminology is foundational to immunology and pathology, describing the initial chemical communication system of the innate immune response. The concept emerged from the discovery of these signaling molecules and their potent, wide-ranging effects on fever, vascular permeability, and the recruitment of immune cells.
Mechanism
The presence of pathogens or damaged tissue components triggers the activation of pattern recognition receptors on immune cells, which in turn activate the nuclear factor kappa B (NF-κB) transcription pathway. This activation drives the rapid gene expression and subsequent release of pro-inflammatory cytokines into the local environment and the systemic circulation. These cytokines then act on distant tissues, including the hypothalamus to induce fever, and the liver to initiate the acute phase protein response.
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