Interferons (IFNs) are produced as a result of the intricate molecular cascade that is triggered during inflammatory processes. They play critical roles in regulating proliferation, differentiation, survival and effector functions of immune and non-immune cell types. IFNs are divided into three classes: type I IFNs (comprised of IFN-as, -ß and others), type II IFNs (IFN-?) and a more recently discovered class called type III IFNs or IFN-?1-3 (also known as IL29, IL28A-B) and IFN-?4 (only IFN-?2 and 3 are present in mice). IFN-?s are recognized by the IFN-? receptor (IFNLR), which is a heterodimer comprising IL-10RB (shared by the IL-10 cytokine family) and IFNLR1 (that confers recognition specificity for IFN-?s) chains.
The IFNLR is distinct from the ubiquitous receptors for type I and II IFNs in that it has a very restricted pattern of expression, being primarily by epithelial cells and by a limited array of immune cells. The IFNLR was originally thought to signal through the same JAK/STAT members also used by the receptor for IFN-a/ß - this is why the IFN-?s, when initially discovered, were believed to have functions that were redundant with those of IFN-a/ß. Recently, however, a series of elegant studies demonstrated that IFN-?s have unique functions relative to IFN-a/ß in terms of maintaining stromal cell resistance and homeostasis in response to viral infections or in the context of inflammation-driven pathologies. Nevertheless, how cells that have the potential to respond to IFN-a/ß also require signaling by IFN-?s to efficiently react to different inflammatory challenges has not yet been settled. Recent work has also shown that type I and III IFNs are not co-regulated as once thought, and that IFN-?s can be induced via distinct signaling pathways.
This Research Topic discusses the regulatory mechanisms that lead to type III IFN expression, and aims to dissect the non-redundant roles played by IFN-?s by non-immune and immune cells in the context of microbial and non-microbial driven inflammatory processes, with special emphasis on the peculiar responses associated with the IFN-? signaling cascade.
Interferons (IFNs) are produced as a result of the intricate molecular cascade that is triggered during inflammatory processes. They play critical roles in regulating proliferation, differentiation, survival and effector functions of immune and non-immune cell types. IFNs are divided into three classes: type I IFNs (comprised of IFN-as, -ß and others), type II IFNs (IFN-?) and a more recently discovered class called type III IFNs or IFN-?1-3 (also known as IL29, IL28A-B) and IFN-?4 (only IFN-?2 and 3 are present in mice). IFN-?s are recognized by the IFN-? receptor (IFNLR), which is a heterodimer comprising IL-10RB (shared by the IL-10 cytokine family) and IFNLR1 (that confers recognition specificity for IFN-?s) chains.
The IFNLR is distinct from the ubiquitous receptors for type I and II IFNs in that it has a very restricted pattern of expression, being primarily by epithelial cells and by a limited array of immune cells. The IFNLR was originally thought to signal through the same JAK/STAT members also used by the receptor for IFN-a/ß - this is why the IFN-?s, when initially discovered, were believed to have functions that were redundant with those of IFN-a/ß. Recently, however, a series of elegant studies demonstrated that IFN-?s have unique functions relative to IFN-a/ß in terms of maintaining stromal cell resistance and homeostasis in response to viral infections or in the context of inflammation-driven pathologies. Nevertheless, how cells that have the potential to respond to IFN-a/ß also require signaling by IFN-?s to efficiently react to different inflammatory challenges has not yet been settled. Recent work has also shown that type I and III IFNs are not co-regulated as once thought, and that IFN-?s can be induced via distinct signaling pathways.
This Research Topic discusses the regulatory mechanisms that lead to type III IFN expression, and aims to dissect the non-redundant roles played by IFN-?s by non-immune and immune cells in the context of microbial and non-microbial driven inflammatory processes, with special emphasis on the peculiar responses associated with the IFN-? signaling cascade.
