Immune-Mediated Repair: A Matter of Plasticity

Laurent, Paôline; Jolivel, Valérie; Manicki, Pauline; Chiu, Lynn; Contin‐Bordes, Cécile; Truchetet, M.-E.; Pradeu, Thomas

doi:10.3389/fimmu.2017.00454

Cited by 49 publications

(47 citation statements)

References 111 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Thus, the issue is not whether Tregs are central to tissue repair but how Treg exert regulatory effects within different local microenvironments. For example, there is a tightly regulated immune cell network encompassing Tregs and macrophages that promotes repair by a cytokine-mediated pathway [46, 90]. A better understanding of the intimate relationship among Tregs, other immune cells and relevant tissue cells will provide clues to the pathology involved in tissue damage and repair.…”

Section: Resultsmentioning

confidence: 99%

‘Repair’ Treg Cells in Tissue Injury

Zhang

Feng

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Studies in mice and humans have elucidated an important role for Tregs in promoting tissue repair and restoring tissue integrity. Emerging evidence has revealed that Tregs promoted wound healing and repair processes at multiple tissue sites, such as the heart, liver, kidney, muscle, lung, bone and central nervous system. The localization of repair Tregs in the lung, muscle and liver exhibited unique phenotypes and functions. Epidermal growth factor receptor, amphiregulin, CD73/CD39 and keratinocyte growth factor are important repair factors that are produced or expressed by repair Tregs; these factors coordinate with parenchymal cells to limit injury and promote repair. In addition, repair Tregs can be modulated by IL-33/ST2, TCR signals and other cytokines in the context of injured microenvironment cues. In this review, we provide an overview of the emerging knowledge about Treg-mediated repair in damaged tissues and organs.

show abstract

Section: Resultsmentioning

confidence: 99%

‘Repair’ Treg Cells in Tissue Injury

Zhang

Feng

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Intra-lineage plasticity, defined as phenotypic and functional changes occurring within a given cell lineage, 23 remains largely understudied in the context of NK cells. Most studies published so far have examined dynamic phenotypic changes in the NK cell repertoire in a tumor setting, either using mouse models or stimulation with tumor cell lines 25,31 .…”

Section: Discussionmentioning

confidence: 99%

“…Intra-lineage cell plasticity, also known as functional plasticity, is the term describing phenotypic and functional changes occurring within a given cell lineage 23 . Functional plasticity is an adaptation of the immune system to its surroundings, for examples transition between M1 and M2 phenotypes in macrophages, transition between ILC1, ILC2 and ILC3 or transition between…”

Section: Introductionmentioning

confidence: 99%

Intra-lineage Plasticity and Functional Reprogramming Maintain Natural Killer Cell Repertoire Diversity

Pfefferle

Jacobs

Ask

et al. 2019

Preprint

View full text Add to dashboard Cite

One Sentence Summary: High-resolution flow cytometry combined with single-cell RNA sequencing reveal a role for intra-lineage plasticity and functional reprogramming in maintaining phenotypically and functionally diverse NK cell repertoires during IL-15-driven homeostatic proliferation. 2 Abstract Natural killer (NK) cell repertoires are made up of a vast number of phenotypically distinct subsets with different functional properties. The molecular programs involved in maintaining NK cell repertoire diversity under homeostatic conditions remains elusive. Here we show that subsetspecific NK cell proliferation kinetics correlate with mTOR activation, and that global repertoire diversity is maintained through a high degree of intra-lineage subset plasticity during IL-15-driven homeostatic proliferation in vitro. High-resolution flow cytometry and single cell RNA sequencing revealed that slowly cycling sorted KIR + CD56 dim NK cells with an induced CD57 phenotype display increased functional potential associated with inhibitory MHC interactions and activating DAP12 signaling. In contrast, rapidly cycling cells upregulate NKG2A and display a general loss of functionality associated with a transcriptional increase in RNA-binding metabolic enzymes and cytokine signaling pathways. These results shed new light on the role of intra-lineage plasticity during NK cell homeostasis and suggest that the functional fate of the cell is tightly linked to the acquired phenotype and determined by transcriptional reprogramming.

show abstract

“…Ennélfogva a gyulladás fertőzés nélkül is létrejöhet. A gyulladást egyre inkább a szövetintegritás károsítására adott általános reakcióként tartják számon, annak okától függetlenül [61]. Ez megmagyarázza azt a megfigyelést is, hogy a diabetesben előforduló gyulladás az adipocyták stresszéből ered, és nem fertőzés következménye, de mai ismereteink szerint az endometriosisos laesiók által generált gyulladás is mentes a fertőzéstől [62].…”

Section: A Blastocysta Tapadási éS a Beágyazódási Reakciók Molekuláriunclassified

A gyulladásos és immunológiai folyamatok kapcsolata a várandósság alatt. Gyakorlati vonatkozások

2019

View full text Add to dashboard Cite

The aim of this review is to explore, in addition to revealing the biological background, new conceptual and therapeutic approaches for reproductive clinicians to provide better and more effective care for sterile and infertile couples. In humans, 75% of unsuccessful pregnancies are the result of failures of implantation, and implantation failure is the limiting factor for in vitro fertilization treatment. A modified “good” inflammation is necessary for implantation and parturition, but for most of pregnancy, inflammation threatens the continuation of pregnancy. During this period, maintaining the non-inflammatory condition is extremely important, enabling the maternal epigenetic effects to occur in the fetus, making it possible for the offspring to adapt as much as possible to the extrauterine life. In the maintenance of the non-inflammatory condition of pregnancy, a large amount of progesterone hormone produced by the placenta (after the luteo-placental shift) plays a crucial role. It has been reported that the role of inflammation during implantation is an ancestral response to the embryo as a foreign body. During normal pregnancy, this inflammation is initiated by the trophoblast and involves the suppression of neutrophil infiltration, the recruitment of natural killer cells to the site of implantation as well as the production of a range of proinflammatory cytokines. During the “implantation window”, the uterus is primed to produce several inflammatory signals such as prostaglandin E2 and a range of proinflammatory cytokines, including TNF, IL6 and IFNγ. The feto-placental unit is a semi-foreign graft called a “semi allograft”, and the recognition of pregnancy by the mother (host) and the resulting maternal immune tolerance is an essential part of successful pregnancy and the birth of a healthy fetus. Because of the functional or absolute reduction of circulating progesterone (due to the decreasing hormone production of the physiologically “aging” placenta after around the 36th week of pregnancy) progesterone effects become insufficient. Therefore it is unable to suppress the production of IL8 and other inflammatory cytokines and the term inflammation, leading to cervical ripening, uterus contractions and parturition (“good” inflammation). Orv Hetil. 2019; 160(32): 1247–1259.

show abstract

Immune-Mediated Repair: A Matter of Plasticity

Cited by 49 publications

References 111 publications

‘Repair’ Treg Cells in Tissue Injury

‘Repair’ Treg Cells in Tissue Injury

Intra-lineage Plasticity and Functional Reprogramming Maintain Natural Killer Cell Repertoire Diversity

A gyulladásos és immunológiai folyamatok kapcsolata a várandósság alatt. Gyakorlati vonatkozások

Contact Info

Product

Resources

About