Mechanism of Graft Damage Caused by NTPDase1-activated Macrophages in Acute Antibody-Mediated Rejection

Xue, Peng; Zhang, Yong; Wang, Xiaoyan; Yuanshan, Cui; Wei, Guangzhu; Liu, Xuehuan

doi:10.1016/j.transproceed.2020.06.033

Cited by 4 publications

(4 citation statements)

References 12 publications

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“…Although the macrophage-mediated release of pro-inflammatory cytokines, such as IL-6 and TNF-α following the allorecognition facilitates T-cell responses in transplant rejection [ 241 , 253 ]. Peng et al demonstrated that macrophages can also produce B-cell activating factor (BAFF), resulting in graft damage during the antibody mediated rejection [ 243 , 254 ].…”

Section: M1/m2 Macrophages In Transplantationmentioning

confidence: 99%

M1/M2 macrophages and their overlaps – myth or reality?

Strizova,

Benesova,

Bartolini

et al. 2023

Clinical Science

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Macrophages represent heterogeneous cell population with important roles in defence mechanisms and in homoeostasis. Tissue macrophages from diverse anatomical locations adopt distinct activation states. M1 and M2 macrophages are two polarized forms of mononuclear phagocyte in vitro differentiation with distinct phenotypic patterns and functional properties, but in vivo, there is a wide range of different macrophage phenotypes in between depending on the microenvironment and natural signals they receive. In human infections, pathogens use different strategies to combat macrophages and these strategies include shaping the macrophage polarization towards one or another phenotype. Macrophages infiltrating the tumours can affect the patient’s prognosis. M2 macrophages have been shown to promote tumour growth, while M1 macrophages provide both tumour-promoting and anti-tumour properties. In autoimmune diseases, both prolonged M1 activation, as well as altered M2 function can contribute to their onset and activity. In human atherosclerotic lesions, macrophages expressing both M1 and M2 profiles have been detected as one of the potential factors affecting occurrence of cardiovascular diseases. In allergic inflammation, T2 cytokines drive macrophage polarization towards M2 profiles, which promote airway inflammation and remodelling. M1 macrophages in transplantations seem to contribute to acute rejection, while M2 macrophages promote the fibrosis of the graft. The view of pro-inflammatory M1 macrophages and M2 macrophages suppressing inflammation seems to be an oversimplification because these cells exploit very high level of plasticity and represent a large scale of different immunophenotypes with overlapping properties. In this respect, it would be more precise to describe macrophages as M1-like and M2-like.

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Section: M1/m2 Macrophages In Transplantationmentioning

confidence: 99%

M1/M2 macrophages and their overlaps – myth or reality?

Strizova,

Benesova,

Bartolini

et al. 2023

Clinical Science

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“…Recently, Peng et al (2021) investigated the correlation between the NTPDase1 expression level and the degree of skin graft injuries in a mice model. They found a negative correlation showing that the higher the expression of the NTPDase1, the lower the concentration of extracellular ADP, proliferation and activation of macrophages and B cells activity.…”

Section: Discussionmentioning

confidence: 99%

“…They found a negative correlation showing that the higher the expression of the NTPDase1, the lower the concentration of extracellular ADP, proliferation and activation of macrophages and B cells activity. Thus, the activity of NTPDase1 was able to decrease the degree of skin graft injuries, providing a foundation for new studies investigating the use of NTPDase1 to alleviate organ damage, during the acute Antibody‐mediated rejection (Peng et al 2021). Therefore, NTPDase1 expression could be associated with immunogenic events in tissue regeneration.…”

Section: Discussionmentioning

confidence: 99%

UTP increases wound healing in the self assembled skin substitute (SASS)

Naasani

Sévigny

Moulin

et al. 2023

J. Cell Commun. Signal.

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The therapeutic potential of purinergic signaling has been explored for a wide variety of diseases, including those related to the skin. In this study, we used the self‐assembled skin substitutes (SASS), a highly functional reconstructed human skin model, which shares many properties with normal human skin, to study the impact of purinergic receptors agonists, such as ATP, UTP and a P2Y receptor antagonist, Reactive Blue 2 during wound healing. After treating the wounded skins, we evaluated the wound area, reepithelialization, length of migrating tongues toward the wound, quality of the skins through the cytokeratin 10 and laminin‐5 expression, epidermal and dermal cell proliferation. In addition, the expression of the main ectoenzymes capable of hydrolyzing nucleotides were investigated through the wounded SASS regions: unwounded region, wound margin, intermediate region and migrating epidermal tongue. After 3 days, under the UTP treatment, the wounded SASS showed an increase in the reepithelialization and in the proliferation of keratinocytes and fibroblasts, without altering the quality of the skin. We also identified the presence of the ectoenzymes NTPDase1 and NPP1 in the reconstructed human skin model, suggesting their involvement in wound healing. Considering the need for new therapies capable of promoting healing in complex wounds, although these results are still preliminary, they suggest the involvement of extracellular nucleotides in human skin healing and the importance to understand their role in this mechanism. New experiments it will be necessary to determine the mechanisms by which the purinergic signaling is involved in the skin wound healing.

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“…Thus, B cells have been demonstrated to promote allograft fibrosis. In a mouse skin graft model, activated MHC II high macrophages produce B cell activating factor (BAFF), which activates B cells to secrete DSA, leading to graft damage in AMR [ 80 ]. Moreover, cardiac allografts from murine recipients treated with MHC I DSA promoted monocyte differentiation into CD68 + CD206 + M2 macrophages in the endothelium of grafts [ 81 ].…”

Section: Interaction Of Recipient-derived Macrophages With Adaptive I...mentioning

confidence: 99%

Intragraft immune cells: accomplices or antagonists of recipient-derived macrophages in allograft fibrosis?

Zhu

et al. 2023

Cell. Mol. Life Sci.

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Organ fibrosis caused by chronic allograft rejection is a major concern in the field of transplantation. Macrophage-to-myofibroblast transition plays a critical role in chronic allograft fibrosis. Adaptive immune cells (such as B and CD4+ T cells) and innate immune cells (such as neutrophils and innate lymphoid cells) participate in the occurrence of recipient-derived macrophages transformed to myofibroblasts by secreting cytokines, which eventually leads to fibrosis of the transplanted organ. This review provides an update on the latest progress in understanding the plasticity of recipient-derived macrophages in chronic allograft rejection. We discuss here the immune mechanisms of allograft fibrosis and review the reaction of immune cells in allograft. The interactions between immune cells and the process of myofibroblast formulation are being considered for the potential therapeutic targets of chronic allograft fibrosis. Therefore, research on this topic seems to provide novel clues for developing strategies for preventing and treating allograft fibrosis.

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Mechanism of Graft Damage Caused by NTPDase1-activated Macrophages in Acute Antibody-Mediated Rejection

Cited by 4 publications

References 12 publications

M1/M2 macrophages and their overlaps – myth or reality?

M1/M2 macrophages and their overlaps – myth or reality?

UTP increases wound healing in the self assembled skin substitute (SASS)

Intragraft immune cells: accomplices or antagonists of recipient-derived macrophages in allograft fibrosis?

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