In recent years, the published literature has suggested the key involvement of the cytokine interleukin-31 (IL-31) in the symptomatology of pruritus, and both IL-31 and its receptor have become potential therapeutic targets for a range of pruritic diseases. Elevated levels of IL-31 or its receptor have been reported in the tissue or serum of patients with pruritic skin diseases, such as atopic dermatitis, prurigo nodularis, and psoriasis. Pruritus places a heavy burden on patients, and can have a negative impact on daily life, sleep, and mental health. Since current anti-pruritic treatments are often ineffective, affected patients are in urgent need of new therapies. As a result, drug development targeting the IL-31 pathway is evolving rapidly. To date, only nemolizumab, a humanized monoclonal antibody targeting the IL-31 receptor, has successfully completed late-stage clinical studies. This article will highlight our current clinical understanding of the role of IL-31 in pruritic disease, and explore recent progress in drug development as well as the anticipated future advances in this field.
Innate Lymphoid cells (ILCs) are tissue resident immune cells which have been recently implicated in initiating and driving anti-tumor responses. ILCs are classified into three main groups, namely type 1 ILCs (ILC1), type 2 ILCs and type 3 ILCs. All three groups have been implicated in either eliciting pro or anti-tumor immune responses in different cancer subtypes with the consensus that ILCs cannot be overlooked within the field of anti-tumor immune responses. In this review we will specifically expand on the knowledge on ILC1, their characterization, function, and plasticity in anti-cancer immune responses. Within this premise, we will discuss caveats of ILC1 characterization, and expand on the expression and function of immune checkpoint receptors within ILC1 subsets, specifically focusing on the role of programmed cell death-1 receptor in controlling specific ILC1 responses. We summarize that ILC1s are a vital component in initiating anti-tumor responses and can be boosted by checkpoint receptors.
The cGAS-STING pathway is an evolutionarily conserved immune signaling pathway critical for microbial defense. Unlike other innate immune pathways that largely rely on stationary cascades of signaling events, STING is highly mobile in the cell. STING is activated on the ER, but only signals after it …
Abstract. Innate Lymphoid cells (ILCs) are tissue resident immune cells which have been recently implicated in initiating and driving anti-tumor responses. ILCs
Support us on Patreon: https://www.patreon.com/InsideTheHiveTV Beekeeping technologies videos - https://bit.ly/2Z03HKA Dalan Animal health: https://www.dalan.com/ _______________________________________________________________ Honey bee immune system overview. Honey bee vaccine on the way? Dalan animal health. In this video, I give you a short overview of the immune system of Honey bees and tell you how the sponsor of the video Dalan Animal health is taking advantage of this research area to develop the first honey bee vaccine ever. Very interesting subject and I hope you enjoy it.
I plan to bring the researchers involved in this project to one of my Livestreams and if you want to ask a question and participate sign up to our email list to receive updates on when the event will happen. Newsletters: https://bit.ly/2LVB5iI
Here is the article that started the idea about a vaccine: "Transfer of Immunity from Mother to Offspring Is Mediated via Egg-Yolk Protein Vitellogenin" Authors: Heli Salmela, Gro V. Amdam, Dalial Freitak https://doi.org/10.1371/journal.ppat.1005015
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A research team led by UCLA Jonsson Comprehensive Cancer Center scientists has identified and analyzed the steps by which immune cells “see” and respond to cancer cells. Their findings may lead to more personalized immunotherapies for patients whose immune systems do not appear to respond to treatment.
A preprint by Le Coz et al. identifies that human T follicular regulatory cells with differences in T cell suppressive and B cell helper capacities can be derived from the regulatory T cell lineage or the T follicular helper cell lineage.
Summary. Interleukin (IL)-33 is highly expressed in the nucleus of cells present at barrier sites and signals via the ST2 receptor. IL-33 signalling via ST2 is
Non-hematopoietic lymphoid stromal cells (LSC) maintain lymph node architecture and form niches allowing the migration, activation, and survival of immune cells. Depending on their localization in the lymph node, these cells display heterogeneous properties and secrete various factors supporting the different activities of the adaptive immune response. LSCs participate in the transport of antigen from the afferent lymph as well as in its delivery into the T and B cell zones and organize cell migration via niche-specific chemokines. While marginal reticular cells (MRC) are equipped for initial B-cell priming and T zone reticular cells (TRC) provide the matrix for T cell-dendritic cell interactions within the paracortex, germinal centers (GC) only form when both T- and B cells successfully interact at the T-B border and migrate within the B-cell follicle containing the follicular dendritic cell (FDC) network. Unlike most other LSCs, FDCs are capable of presenting antigen via complement receptors to B cells, which then differentiate within this niche and in proximity to T follicular helper (TFH) cells into memory and plasma cells. LSCs are also implicated in maintenance of peripheral immune tolerance. In mice, TRCs induce the alternative induction of regulatory T cells instead of TFH cells by presenting tissue-restricted self-antigens to naïve CD4 T cells via MHC-II expression. This review explores potential implications of our current knowledge of LSC populations regardin
The induction of proinflammatory T cells by dendritic cell (DC) subtypes is critical for antitumor responses and effective immune checkpoint blockade (ICB) therapy.Here, we show that human CD1c<sup>+</sup>CD5<sup>+</sup> DCs are reduced in melanoma-affected lymph nodes, with CD5 expression on DCs...
COVID-19 patients have reduced thymic T- cell output, and disease severity negatively correlates with thymic function. SARS-CoV-2 targeting of thymic epithelial cells induces the downregulation of critical pathways associated with epithelial cell adhesion and survival.
Triggering receptors expressed on myeloid cells (TREMs) encompass a family of cell-surface receptors chiefly expressed by granulocytes, monocytes and tissue macrophages. These receptors have been implicated in inflammation, neurodegenerative diseases, bone remodelling, metabolic syndrome, atherosclerosis and cancer. Here, I review the structure, ligands, signalling modes and functions of TREMs in humans and mice and discuss the challenges that remain in understanding TREM biology. In this Review, Marco Colonna provides a comprehensive summary of the triggering receptor expressed on myeloid cells (TREM) family of receptors. TREMs are important for modulating signalling in myeloid cells and have now been implicated in many different disease settings, including inflammatory diseases, autoimmunity, neurodegeneration and cancer.
Exchange of ideas and information among doctors, nurses, biomedical investigators, patients and their families concerned with primary immunodeficiency diseases (PID).
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