About: Interleukin 30 is a research topic. Over the lifetime, 5 publications have been published within this topic receiving 51 citations. The topic is also known as: IL-27A & IL27A.
TL;DR: The aim of this review was to present a concise version of the information available on these novel cytokines to facilitate their understanding by members of the immunological community.
Abstract: Cytokines are important molecules that regulate the ontogeny and function of the immune system. They are small secreted proteins usually produced upon activation of cells of the immune system, including lymphocytes and myeloid cells. Many cytokines have been described, and several have been recognized as pivotal players in immune responses and in human disease. In fact, several anticytokine antibodies have proven effective therapeutics, especially in various autoimmune diseases. In the last 15 years, new cytokines have been described, and many remain poorly understood. Among the most recent cytokines discovered are interleukins-30 (IL-30) to IL-40. Several of these are members of other cytokine superfamilies, including several IL-1 superfamily members (IL-33, IL-36, IL-37, and IL-38) as well as several new members of the IL-12 family (IL-30, IL-35, and IL-39). The rest (IL-31, IL-32, IL-34, and IL-40) are encoded by genes that do not belong to any cytokine superfamily. Our aim of this review was to present a concise version of the information available on these novel cytokines to facilitate their understanding by members of the immunological community.
TL;DR: It is demonstrated that like IL-27, IL-30 upregulated TLR4 expression to enhance lipopolysaccharide-induced TNF-α production in human monocytes and required WSX-1 engagement and signal transducer and activator of transcription (STAT) 3 phosphorylation.
Abstract: Interleukin (IL)-30, the IL-27p28 subunit of the heterodimeric cytokine IL-27, acts as an antagonist of IL-27 and IL-6 signaling in murine cells via glycoprotein 130 (gp130) receptor and additional binding partners. Thus far, functions of IL-30 have not been fully elucidated in human cells. We demonstrate that like IL-27, IL-30 upregulated TLR4 expression to enhance lipopolysaccharide-induced TNF-α production in human monocytes; however, these IL-30-mediated activities did not reach the same levels of cytokine induction compared to IL-27. Interestingly, IL-30- and IL-27-mediated interferon-γ-induced protein 10 (IP-10) production required WSX-1 engagement and signal transducer and activator of transcription (STAT) 3 phosphorylation; furthermore, IL-30 induced STAT phosphorylation after 16 h, whereas IL-27 induced STAT phosphorylation within 30 min. This prompted us to examine if a secondary mediator was required for IL-30-induced pro-inflammatory functions, and hence we examined IL-6-related molecules. Combined with inhibition of soluble IL-6 receptor α (sIL-6Rα) and data showing that IL-6 inhibited IL-30/IL-27-induced IP-10 expression, we demonstrate a role for sIL-6Rα and gp130 in IL-30-mediated activity in human cells.
TL;DR: The mechanisms whereby IL-30 amplifies intratumoral myeloid cell infiltrate and triggers a vicious cycle that worsens immunosuppression in the tumor microenvironment (TME) and constitutes a real threat for a successful immunotherapeutic strategy are focused on.
Abstract: In the last few years, a new actor hit the scene of the tumor microenvironment, the p28 subunit of interleukin (IL)-27, known as IL-30. Its molecular structure allows it to function as an autonomous cytokine and, alternatively, to pair with other subunits to form heterodimeric complexes and enables it to play different, and not fully elucidated, roles in immunity. However, data from the experimental models and clinical samples, suggest IL-30's engagement in the relationship between cancer and myeloid cells, which fosters the tumor microenvironment and the cancer stem cell niche, boosting the disease progression. Activated myeloid cells are the primary cellular source and one of the targets of IL-30, which can also be produced by cancer cells, especially, in aggressive tumors, as observed in the breast and prostate. This review briefly reports on the immunobiology of IL-30 and related cytokines, by comparing mouse and human counterparts, and then focuses on the mechanisms whereby IL-30 amplifies intratumoral myeloid cell infiltrate and triggers a vicious cycle that worsens immunosuppression in the tumor microenvironment (TME) and constitutes a real threat for a successful immunotherapeutic strategy.
TL;DR: This poster presents a probabilistic procedure called a “spatially aggregating immune checkpoint blockade” (SCD) assay, which is a very simple and effective way to diagnose and treat central nervous system disorders.
TL;DR: This study supports the functional link between KLB and gallstone disease, as suggested by Zweers et al. and suggests that intestinal hypomotility contributes to gallstone susceptibility in carriers of the KLB risk variant.