Type 3 innate lymphoid cells are associated with a successful intestinal transplant.

MedStar author(s):
Citation: American Journal of Transplantation. 21(2):787-797, 2021 02.PMID: 32594614Institution: MedStar Health Research Institute | MedStar Washington Hospital CenterDepartment: MedStar General Surgery ResidencyForm of publication: Journal ArticleMedline article type(s): Journal Article | Research Support, N.I.H., ExtramuralSubject headings: IN PROCESS -- NOT YET INDEXEDYear: 2021ISSN:
  • 1600-6135
Name of journal: American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant SurgeonsAbstract: Although innate lymphoid cells (ILCs) play fundamental roles in mucosal barrier functionality and tissue homeostasis, ILC-related mechanisms underlying intestinal barrier function, homeostatic regulation, and graft rejection in intestinal transplantation (ITx) patients have yet to be thoroughly defined. We found protective type 3 NKp44+ ILCs (ILC3s) to be significantly diminished in newly transplanted allografts, compared to allografts at 6 months, whereas proinflammatory type 1 NKp44- ILCs (ILC1s) were higher. Moreover, serial immunomonitoring revealed that in healthy allografts, protective ILC3s repopulate by 2-4 weeks postoperatively, but in rejecting allografts they remain diminished. Intracellular cytokine staining confirmed that NKp44+ ILC3 produced protective interleukin-22 (IL-22), whereas ILC1s produced proinflammatory interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha). Our findings about the paucity of protective ILC3s immediately following transplant and their repopulation in healthy allografts during the first month following transplant were confirmed by RNA-sequencing analyses of serial ITx biopsies. Overall, our findings show that ILCs may play a key role in regulating ITx graft homeostasis and could serve as sentinels for early recognition of allograft rejection and be targets for future therapies. Copyright (c) 2020 The American Society of Transplantation and the American Society of Transplant Surgeons.All authors: Belyayev L, Bhuvaneshwar K, Cha P, Fishbein TM, Gusev Y, Hawksworth J, Kaiser J, Kang J, Khan K, Kroemer A, Loh K, Matsumoto CS, Moturi S, Ressom H, Robson SC, Sadat M, Zasloff MFiscal year: FY2021Digital Object Identifier: ORCID: Date added to catalog: 2020-08-26
Holdings
Item type Current library Collection Call number Status Date due Barcode
Journal Article MedStar Authors Catalog Article 32594614 Available 32594614

Although innate lymphoid cells (ILCs) play fundamental roles in mucosal barrier functionality and tissue homeostasis, ILC-related mechanisms underlying intestinal barrier function, homeostatic regulation, and graft rejection in intestinal transplantation (ITx) patients have yet to be thoroughly defined. We found protective type 3 NKp44+ ILCs (ILC3s) to be significantly diminished in newly transplanted allografts, compared to allografts at 6 months, whereas proinflammatory type 1 NKp44- ILCs (ILC1s) were higher. Moreover, serial immunomonitoring revealed that in healthy allografts, protective ILC3s repopulate by 2-4 weeks postoperatively, but in rejecting allografts they remain diminished. Intracellular cytokine staining confirmed that NKp44+ ILC3 produced protective interleukin-22 (IL-22), whereas ILC1s produced proinflammatory interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha). Our findings about the paucity of protective ILC3s immediately following transplant and their repopulation in healthy allografts during the first month following transplant were confirmed by RNA-sequencing analyses of serial ITx biopsies. Overall, our findings show that ILCs may play a key role in regulating ITx graft homeostasis and could serve as sentinels for early recognition of allograft rejection and be targets for future therapies. Copyright (c) 2020 The American Society of Transplantation and the American Society of Transplant Surgeons.

English

Powered by Koha