Cytotoxic Responses Mediated by NK Cells and Cytotoxic T Lymphocytes in Xenotransplantation.

IF 2.7 3区医学 Q1 SURGERY

Transplant International Pub Date : 2025-02-12 eCollection Date: 2025-01-01 DOI:10.3389/ti.2025.13867

Viktoriia Galdina, Gisella L Puga Yung, Jörg D Seebach

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Abstract

Xenotransplantation represents a potential solution to the shortage of organs for transplantation. The recent advancements in porcine genetic modification have addressed hyperacute and acute vascular rejection; however, challenges persist with regard to delayed xenograft rejection. Porcine endothelial cells (pECs) represent a crucial target in the context of xenograft rejection, which is mediated by cytotoxic lymphocytes. It is crucial to comprehend the manner in which human natural killer (NK) cells and cytotoxic CD8⁺ T lymphocytes (CTL) recognize and target pECs in order to develop efficacious prophylactic strategies against rejection. The objective of the present review is to synthesize the existing knowledge regarding the mechanisms and techniques employed to modulate xenogeneic responses mediated by human NK cells and CTL. We will elucidate recent methodological advancements, debate potential novel strategies, and emphasize the imperative necessity for further research and innovative approaches to enhance graft survival.

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来源期刊

Transplant International 医学-外科

CiteScore

4.70

自引率

6.50%

发文量

211

审稿时长

3-8 weeks

期刊介绍： The aim of the journal is to serve as a forum for the exchange of scientific information in the form of original and high quality papers in the field of transplantation. Clinical and experimental studies, as well as editorials, letters to the editors, and, occasionally, reviews on the biology, physiology, and immunology of transplantation of tissues and organs, are published. Publishing time for the latter is approximately six months, provided major revisions are not needed. The journal is published in yearly volumes, each volume containing twelve issues. Papers submitted to the journal are subject to peer review.