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Type 2 immunity and wound healing: evolutionary refinement of adaptive immunity by helminths

TLDR
The relationship between the control of helminth infection and the mechanisms of wound repair is examined, and a new understanding of the adaptive type 2 immune response and its contribution to both host tolerance and resistance is provided.
Abstract
In this Opinion, the authors provide their perspective on how the type 2 immune response may have evolved and how it functions to mediate both resistance and tolerance to tissue-destructive helminths They propose that the damage induced during helminth migration and the subsequent need for tissue repair have been major factors in driving the evolution of the type 2 response

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Control of adaptive immunity by the innate immune system

TL;DR: These emerging principles of innate control of adaptive immunity are discussed, which are variations on a common design principle wherein the cells that sense infections produce one set of cytokines to induce lymphocytes to produce another set ofinflammatory cytokines, which in turn activate effector responses.
Journal ArticleDOI

Cell-intrinsic lysosomal lipolysis is essential for alternative activation of macrophages

TL;DR: In this article, the authors found that the uptake of triacylglycerol substrates via the scavenger receptor CD36 and their subsequent lipolysis by lysosomal acid lipase (LAL) was important for the engagement of elevated oxidative phosphorylation, enhanced spare respiratory capacity (SRC), prolonged survival and expression of genes that together define M2 activation.

Cell-intrinsic lysosomal lipolysis is essential for macrophage alternative activation

TL;DR: It is found that the uptake of triacylglycerol substrates via the scavenger receptor CD36 and their subsequent lipolysis by lysosomal acid lipase (LAL) was important for the engagement of elevated oxidative phosphorylation, enhanced spare respiratory capacity (SRC), prolonged survival and expression of genes that together define M2 activation.
Journal ArticleDOI

Type 2 cytokines: mechanisms and therapeutic strategies

TL;DR: The many endogenous negative regulatory mechanisms that antagonize type 2 immunity are discussed and how therapies that target some of these pathways are being developed to treat type 2-mediated disease are highlighted.
References
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Journal ArticleDOI

Exploring the full spectrum of macrophage activation.

TL;DR: This Review suggests a new grouping of macrophages based on three different homeostatic activities — host defence, wound healing and immune regulation, and proposes that similarly to primary colours, these three basic macrophage populations can blend into various other 'shades' of activation.
Journal ArticleDOI

Mechanisms of fibrosis: therapeutic translation for fibrotic disease

TL;DR: How cell-intrinsic changes in important structural cells can perpetuate the fibrotic response by regulating the differentiation, recruitment, proliferation and activation of extracellular matrix–producing myofibroblasts is described.
Journal ArticleDOI

Wound healing: an overview of acute, fibrotic and delayed healing.

TL;DR: This review describes the major biological processes associated with both normal and pathologic healing of acute wounds, characterized by four distinct, but overlapping phases: hemostasis, inflammation, proliferation and remodeling.
Journal ArticleDOI

Nuocytes represent a new innate effector leukocyte that mediates type-2 immunity

TL;DR: The identification and functional characterization of a new innate type-2 immune effector leukocyte that is named the nuocyte is presented, which represents a critically important innate effector cell in type- 2 immunity.
Journal ArticleDOI

Inflammation in wound repair: molecular and cellular mechanisms.

TL;DR: Cellular and molecular mechanisms controlling inflammation in cutaneous tissue repair are reviewed and a rationale for targeting the inflammatory phase in order to modulate the outcome of the healing response is provided.
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