Cytokines at the Edge between Alarm and Homeostasis

Dear Colleagues,

Cytokines are small proteins that play a role in cell signaling. They are called cytokines, chemokines, interferons and interleukins. Cytokines are produced by a broad range of cells, including immune cells as well as structural cells like epithelial cells and they act through specific receptors on the target cell. They can induce differentiation of cells, activation, immunosuppression or migration from different organs and translate information from cell to cell creating an imprint also called memory to distinguish dangerous signals coming from the environment of the host. In the case of inflammation, a new class of cytokines called alarmins was described. They have both chemotactic and immune activating functions and are released as a result of cell injury or death and are thus released mainly at the mucosal site. Alarmins function as intercellular signals by interacting with chemotactic and pattern recognition receptors (PRRs) to activate immune cells in host defense. Alarmins are released in excess by severe injuries, environmental exposure to toxic substances or infectious agents and upon maximal stimulation, they translate this signal into a dangerous effect with potentially lethal cytokine storm. Moreover, as alarmins are a chemoattractant for leukocytes, they can lead to a massive inflammatory response. However, the role of alarmin does not always result in host damage but they can be involved in the clearance of parasites or viruses and other infectious agents. Chronic inflammation thus develops when the host is not able to limit the excess of alarmins triggered from the environment such as in exposure to allergen and/or infection which affect the sensitivity of the homeostatic mechanisms of the host resulting in pathologic alarm without resolving the inflammation. The homeostatic mechanisms of the host are multiple and many of them probably develop as a new adaptive mechanism of the host to survive. There are evidence that cytokines and chemokines long recognized as pro-inflammatory can promote the resolution of the inflammation as we recently discovered for IL-3. We must also consider the origin of the insults targeting simultaneously multiple organs or mucosal sites. This special topic aims to identify new cytokine-chemokine mediated homeostatic mechanisms activated by the host to maintain the homeostatic stage and thus be able to resolve inflammation. This should lead to improvement of current therapeutic strategies for inflammatory diseases.

Prof. Dr. Susetta Finotto
Guest Editor

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• cytokines
• interferons
• alarmins
• chemokines
• cell trafficking
• inflammation
• immunosuppression
• T cells
• eosinophils
• epithelial cells
• homeostasis
• infection