ResearchPad - special-feature-review https://www.researchpad.co Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[Serum IgA Fc effector functions in infectious disease and cancer]]> https://www.researchpad.co/article/elastic_article_8248 The role of mucosal immunoglobulin A (IgA) in infection (e.g. neutralization) has been extensively investigated; by contrast, serum IgA is poorly understood. Crosslinking of serum IgA with fragment crystallizable alpha receptor I (FcαRI) can activate immune cells (e.g. phagocytosis, antibody‐dependent cellular cytotoxicity, reactive oxygen species) to clear select bacteria, viruses and tumors, whereas monomeric serum IgA can inhibit these functions hindering an effective immune response. Here we discuss serum IgA Fc effector functions in infectious disease and tumor clearance, potential applications in immunotherapy and limitations of current research.

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<![CDATA[UV radiation recruits CD4+GATA3+ and CD8+GATA3+ T cells while altering the lipid microenvironment following inflammatory resolution in human skin in vivo ]]> https://www.researchpad.co/article/Nf920785c-d0a3-455d-9cf5-1f057549dab4

Abstract

Objectives

Solar ultraviolet radiation (UVR) has major adverse effects on human health. While the mechanisms responsible for induction of UVR‐induced inflammation are well‐documented, the mediation of its resolution and longer‐term adaptive homeostasis is unknown. Therefore, we examined the skin immune and lipid profile over time following UVR inflammation.

Methods

To investigate the self‐resolving events of UVR inflammation in vivo, human skin was exposed to a single pro‐inflammatory dose of UVR. Skin biopsies and suction blister fluid were taken at intervals up to 2 weeks post‐UVR. The immune infiltrate was quantified by immunohistochemistry, and lipid mediators were profiled by liquid chromatography/mass spectrometry.

Results

We identified that cellular resolution events including switching of macrophage phenotype apply to human sunburn. However, UVR‐induced inflammation in humans involves a post‐resolution phase that differs from other experimental models. We demonstrate that 2 weeks after the initiating UVR stimulus, there is considerable immune activity with CD8+GATA3+ T cells maintained in human skin. Our results challenge the dogma of CD4+FOXP3+ T cells being the main effector CD4+ T‐cell population following UVR, with CD4+GATA3+ T cells the dominant phenotype. Furthermore, lipid mediators are elevated 14 days post‐UVR, demonstrating the skin lipid microenvironment does not revert to the tissue setting occurring prior to UVR exposure.

Conclusion

We have identified for the first time that CD4+GATA3+ and CD8+GATA3+ T‐cell subpopulations are recruited to UVR‐inflamed human skin, demonstrating discrepancies between the adaptive UVR response in mice and humans. Future strategies to abrogate UVR effects may target these T‐cell subpopulations and also the persistent alteration of the lipid microenvironment post‐UVR.

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<![CDATA[Mucins and their receptors in chronic lung disease]]> https://www.researchpad.co/article/Ne5d98293-d7f4-4236-86d5-48d03bda2b1f

Abstract

There is growing recognition that mucus and mucin biology have a considerable impact on respiratory health, and subsequent global morbidity and mortality. Mucins play a critical role in chronic lung disease, not only by providing a physical barrier and clearing pathogens, but also in immune homeostasis. The aim of this review is to familiarise the reader with the role of mucins in both lung health and disease, with particular focus on function in immunity, infection and inflammation. We will also discuss their receptors, termed glycan‐binding proteins, and how they provide an attractive prospect for therapeutic intervention.

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<![CDATA[Primate thanatology and hominoid mortuary archeology]]> https://www.researchpad.co/article/N8ff7f3d2-a335-42e1-b6ba-ada109405595

In recent years, a thanatology of primates has become a respectable research topic, and although still sparse, observations among several taxa have shown how complex responses to the dead can be. In human evolutionary archeology, re-analysis of old ‘burial’ sites is slowly revising our view on the development of specifically human responses to the dead. We propose here the means of integrating information from the two disciplines of primatology and archeology, in support of the field of primate thanatology. We propose a terminology and a shared set of research questions, from which we generate a number of observations that can be utilized in the field, in order to establish a working dialogue and foster greater collaboration across the two disciplines.

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<![CDATA[The clock is ticking: the impact of ageing on T cell metabolism]]> https://www.researchpad.co/article/Ncbb0e73b-73c3-456e-b1a3-3bede6f50ecd

Abstract

It is now clear that access to specific metabolic programmes controls the survival and function of various immune cell populations, including T cells. Efficient naïve and memory T cell homoeostasis requires the use of specific metabolic pathways and differentiation requires rapid and dramatic metabolic remodelling. While we are beginning to appreciate the crucial role of metabolic programming during normal T cell physiology, many of the potential impacts of ageing on metabolic homoeostasis and remodelling in T cells remain unexplored. This review will outline our current understanding of T cell metabolism and explore age‐related metabolic changes that are postulated or have been demonstrated to impact T cell function.

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<![CDATA[Recent novel approaches to limit oxidative stress and inflammation in diabetic complications]]> https://www.researchpad.co/article/5bfe2bf3d5eed0c4848709c1

Abstract

Diabetes is considered a major burden on the healthcare system of Western and non‐Western societies with the disease reaching epidemic proportions globally. Diabetic patients are highly susceptible to developing micro‐ and macrovascular complications, which contribute significantly to morbidity and mortality rates. Over the past decade, a plethora of research has demonstrated that oxidative stress and inflammation are intricately linked and significant drivers of these diabetic complications. Thus, the focus now has been towards specific mechanism‐based strategies that can target both oxidative stress and inflammatory pathways to improve the outcome of disease burden. This review will focus on the mechanisms that drive these diabetic complications and the feasibility of emerging new therapies to combat oxidative stress and inflammation in the diabetic milieu.

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<![CDATA[The role of IL‐22 in the resolution of sterile and nonsterile inflammation]]> https://www.researchpad.co/article/5bfe2bf1d5eed0c484870929

Abstract

In a broad sense, inflammation can be conveniently characterised by two phases: the first phase, which is a pro‐inflammatory, has evolved to clear infection and/or injured tissue; and the second phase concerns regeneration of normal tissue and restitution of normal physiology. Innate immune cell‐derived pro‐inflammatory cytokines and chemokines activate and recruit nonresident immune cells to the site of infection, thereby amplifying the inflammatory responses to clear infection or injury. This phase is followed by a cytokine milieu that promotes tissue regeneration. There is no absolute temporal distinction between these two phases, and cytokines may have dual pleiotropic effects depending on the timing of release, inflammatory microenvironment or concentrations. IL‐22 is a cytokine with reported pro‐ and anti‐inflammatory roles; in this review, we contend that this protein has primarily a function in restitution of normal tissue and physiology.

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