IL1A-Gen

The IL1A gene (IL1A stands for: interleukin 1 alpha) is a protein-coding gene located on chromosome 2q14.1.

The IL1A gene codes for interleukin-1 alpha (IL-1 alpha), a cytokine that is secreted by various cell types of the immune system such as macrophages, monocytes and dendritic cells, but also by fibroblasts and endothelial cells. It owes its name to the fact that it was the first cytokine to be discovered. Interleukin-1alpha is produced in response to bacterial infections (its production is mainly stimulated by LPS, an endotoxin of gram-negative bacteria), the presence of TNF and the interaction of the producing cells with CD4-positive T lymphocytes. Interleuekin-1 alpha has several effects both locally and generally in the body, including the promotion of inflammatory processes in response to bacterial infections such as vasodilation, spasms and fever. It also stimulates the production of prostaglandins by various cell types (muscles, epithelia, etc.), the production of other cytokines such as IL-2 and the activation and recruitment of other cells of the immune system.

After binding to its receptor IL1R1, it forms the high-affinity interleukin-1 receptor complex together with its accessory protein IL1RAP. The signal transmission involves the recruitment of adapter molecules such as MYD88, IRAK1 or IRAK4 (Cohen I et al. 2015). This in turn mediates the activation of NF-kappa-B and the three MAPK signaling pathways p38, p42/p44 and JNK . Within the cell, it acts as an alarmin and is released into the extracellular space after cell death following rupture of the cell membrane to trigger inflammation and alert the host to injury or damage. In addition to its role as a danger signal that occurs when the cytokine is passively released by cell necrosis, it directly recognizes DNA damage and acts as a signal for genotoxic stress without loss of cell integrity.

Diseases associated with IL1A include cholesteatoma of the middle ear and keratoconjunctivitis sicca. Related signaling pathways include MIF-mediated glucocorticoid regulation and TGF-beta signaling.

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