Transmissible cancers are malignant cells that can spread between individuals of a population, akin to both a parasite and mobile graft. The survival of the Tasmanian devil, the largest remaining marsupial carnivore, is threatened by the remarkable emergence of two independent lineages of transmissible cancer, devil facial tumour (DFT) 1 and devil facial tumour 2 (DFT2). To aid the development of a

The endocrine and the immune systems interact by sharing receptors for hormones and cytokines, cross‐control, and feedback mechanisms. To date, no comprehensive study has assessed the impact of thyroid hormones on immune homeostasis. By studying immune phenotype (cell populations, antibody concentrations, circulating cytokines, adipokines and acute phase proteins, monocyte‐platelet interactions, and

In this issue, we introduce the second part of a series of reviews focusing on how immunometabolism influences host and pathogen interactions during infection. This part of the collection addresses the interface between metabolism and specific types of infection, including immunometabolism in macrophages during helminth infection, the role of metabolism in T‐cell exhaustion during chronic viral infections

In the article by Peruzzi et al.,1 the keywords section was missing on page 345 and should have been added. The keywords should be: Keywords: dendritic cell; neutrophil; viral; inflammation; macrophage. The online version of the article has been corrected.

IL‐33 is a member of the IL‐1 family. By binding to its receptor ST2 (IL‐33R) on mast cells, IL‐33 induces the MyD88‐dependent activation of the TAK1‐IKK2 signalling module resulting in activation of the MAP‐kinases p38, JNK1/2 and ERK1/2, and of NFκB. Depending on the kinases activated in these pathways, the IL‐33‐induced signalling is essential for production of IL‐6 or IL‐2. This was shown to control

Dendritic cells (DCs) play an important role in linking innate and adaptive immunity. DCs can sense endogenous and exogenous antigens and present those antigens to T cells to induce an immune response or immune tolerance. During activation, alternative splicing (AS) in DCs is dramatically changed to induce cytokine secretion and upregulation of surface marker expression. PTBP1, an RNA‐binding protein

During inflammation or tissue injury, pro‐inflammatory mediators attract migratory monocytes to inflammatory sites and monocyte‐to‐macrophage differentiation occurs to activate macrophages. We report here that PAQR11, a member of the progesterone and AdipoQ receptor family, regulates monocyte‐to‐macrophage differentiation in vitro and in vivo. Paqr11 gene was highly induced during monocyte‐to‐macrophage

Trypanosoma cruzi cytosolic tryparedoxin peroxidase (c‐TXNPx) is a 2‐Cys peroxiredoxin (Prx) with an important role in detoxifying host cell oxidative molecules during parasite infection. c‐TXNPx is a virulence factor, since its overexpression enhances parasite infectivity and resistance to exogeneous oxidation. Since Prxs from other organisms possess immunmodulatory properties, we studied the effects

Dysfunction of the immune system underlies a plethora of human diseases, requiring the development of immunomodulatory therapeutic intervention. To date, most strategies employed have been focusing on the modification of T lymphocytes and although remarkable improvement have been obtained, results often fall short of the intended outcome. Recent cutting‐edge technologies have highlighted macrophages

Previously, we demonstrated neuraminidase (NEU) activity or NEU1 expression, specifically, are increased in the kidneys of lupus mice and urine of human patients with nephritis. Additionally, NEU activity mediates IL‐6 secretion from lupus prone MRL/lpr primary mouse mesangial cells (MCs) in response to an IgG mimic. IL‐6 mediates glomerular inflammation and promotes tissue damage in patients and mouse

2020 was a year unlike any other for Immunology. Through the SARS‐CoV‐2 pandemic, with fantastic support from the global immunology community, we worked together to reach new heights. Here, we look back at some of the highlights for Immunology in a challenging and memorable year.

We here introduce a Review Series focussing on the important influences circadian rhythms have on immune responses. The three reviews in this series, expertly curated by Rachel Edgar, discuss how the cyclic oscillations in our cellular clock affect the innate and adaptive immune response, and how interactions with the intestinal microbiota, themselves subject to daily oscillations, also influence immune

Here we announce the first part of an exciting new series of reviews exploring the impact of immunometabolism in the interaction between host and pathogen, and in the outcome of infection. This collection discusses the links between metabolism and epigenetic control of cell function, post‐translation modifications of host proteins that determine protein fate and host cell function, the metabolic determinants

As a distinctive population of leucocytes, innate lymphoid cells (ILCs) participate in immune‐mediated diseases and play crucial roles in tissue remodelling after injury. ILC lineages can be divided into helper ILCs and cytotoxic ILCs. Most helper ILCs are integrated into the fabric of tissues and produce different types of cytokines involving in the pathogenesis of many kinds of cardiovascular disease

Antibodies that bind complement components were first identified over 30 years ago. Investigations into their functions in animal models motivated clinical studies that have now generated licensed products and a strong pipeline of future therapeutics. Despite this, the mechanisms of action of one of the first effective C5‐binding antibodies, BB5.1, were not known. Here, we report a new study that reveals

Our world is changing fast. Microbes, once considered our adversaries, are now recognized as partners. Well, not all microbes, but a vast number that live in the unique niches of our bodies and, in particular, the gut. Recently, we have come to appreciate how our normal microbiota contribute to our health, and how disruption of this partnership can open the way for disease (both infectious and non‐infectious)