Lower expression of NOTCH components in peripheral blood mononuclear cells of allogeneic hematopoietic cell transplant patients

Introduction: Chronic graft-versus-host disease (cGvHD) not only remains the main cause of late mortality after allogeneic hematopoietic cell transplant, but also has the capacity of causing severe organ impairment in those who survive. The Notch, a highly conserved ligand-receptor pathway, is invol...

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Main Authors: Marcos Paulo Colella, Beatriz Corey Morini, Fernanda Niemann, Matheus Rodrigues Lopes, Sara Olalla Saad, Patricia Favaro
Format: Article
Language:English
Published: Elsevier 2023-07-01
Series:Hematology, Transfusion and Cell Therapy
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2531137922000864
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author Marcos Paulo Colella
Beatriz Corey Morini
Fernanda Niemann
Matheus Rodrigues Lopes
Sara Olalla Saad
Patricia Favaro
author_facet Marcos Paulo Colella
Beatriz Corey Morini
Fernanda Niemann
Matheus Rodrigues Lopes
Sara Olalla Saad
Patricia Favaro
author_sort Marcos Paulo Colella
collection DOAJ
description Introduction: Chronic graft-versus-host disease (cGvHD) not only remains the main cause of late mortality after allogeneic hematopoietic cell transplant, but also has the capacity of causing severe organ impairment in those who survive. The Notch, a highly conserved ligand-receptor pathway, is involved in many immunological processes, including inflammatory and regulatory responses. Recently, mouse models have shown that the blockage of canonical Notch signaling prevents GvHD. Objective and Method: Due to the lack of data on the Notch pathway in human chronic GvHD, we sought to study the expression of NOTCH components in primary samples of patients who received allo-HCT and presented active cGvHD or a long-term clinical tolerance to cGvHD. Results: Our results showed a significantly lower expression of NOTCH components in both groups that received allo-HCT, independently of their cGvHD status, when compared to healthy controls. Conclusion: Moreover, there were no differences in gene expression levels between the active cGvHD and clinically tolerant groups. To our knowledge, this is one of the first studies performed in human primary samples and our data indicate that much remains to be learned regarding NOTCH signaling as a new regulator of GvHD.
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spelling doaj.art-83bae80c4f164f57882a2990f27f88f92023-08-30T05:54:32ZengElsevierHematology, Transfusion and Cell Therapy2531-13792023-07-01453324329Lower expression of NOTCH components in peripheral blood mononuclear cells of allogeneic hematopoietic cell transplant patientsMarcos Paulo Colella0Beatriz Corey Morini1Fernanda Niemann2Matheus Rodrigues Lopes3Sara Olalla Saad4Patricia Favaro5Universidade Estadual de Campinas (Unicamp), Campinas, SP, BrazilUniversidade Estadual de Campinas (Unicamp), Campinas, SP, BrazilUniversidade Estadual de Campinas (Unicamp), Campinas, SP, BrazilUniversidade Federal do Vale do São Francisco (Univasf), Paulo Afonso, BA, BrazilUniversidade Estadual de Campinas (Unicamp), Campinas, SP, BrazilUniversidade Estadual de Campinas (Unicamp), Campinas, SP, Brazil; Universidade Federal de São Paulo, (Unifesp), Diadema, SP, Brazil; Corresponding author at: Universidade Federal de São Paulo (UNIFESP), Rua São Nicolau, 210, Diadema, SP, CEP 09913-030, BrazilIntroduction: Chronic graft-versus-host disease (cGvHD) not only remains the main cause of late mortality after allogeneic hematopoietic cell transplant, but also has the capacity of causing severe organ impairment in those who survive. The Notch, a highly conserved ligand-receptor pathway, is involved in many immunological processes, including inflammatory and regulatory responses. Recently, mouse models have shown that the blockage of canonical Notch signaling prevents GvHD. Objective and Method: Due to the lack of data on the Notch pathway in human chronic GvHD, we sought to study the expression of NOTCH components in primary samples of patients who received allo-HCT and presented active cGvHD or a long-term clinical tolerance to cGvHD. Results: Our results showed a significantly lower expression of NOTCH components in both groups that received allo-HCT, independently of their cGvHD status, when compared to healthy controls. Conclusion: Moreover, there were no differences in gene expression levels between the active cGvHD and clinically tolerant groups. To our knowledge, this is one of the first studies performed in human primary samples and our data indicate that much remains to be learned regarding NOTCH signaling as a new regulator of GvHD.http://www.sciencedirect.com/science/article/pii/S2531137922000864NotchChronic graft-versus-host-diseaseAllogeneic hematopoietic cell transplantTolerance
spellingShingle Marcos Paulo Colella
Beatriz Corey Morini
Fernanda Niemann
Matheus Rodrigues Lopes
Sara Olalla Saad
Patricia Favaro
Lower expression of NOTCH components in peripheral blood mononuclear cells of allogeneic hematopoietic cell transplant patients
Hematology, Transfusion and Cell Therapy
Notch
Chronic graft-versus-host-disease
Allogeneic hematopoietic cell transplant
Tolerance
title Lower expression of NOTCH components in peripheral blood mononuclear cells of allogeneic hematopoietic cell transplant patients
title_full Lower expression of NOTCH components in peripheral blood mononuclear cells of allogeneic hematopoietic cell transplant patients
title_fullStr Lower expression of NOTCH components in peripheral blood mononuclear cells of allogeneic hematopoietic cell transplant patients
title_full_unstemmed Lower expression of NOTCH components in peripheral blood mononuclear cells of allogeneic hematopoietic cell transplant patients
title_short Lower expression of NOTCH components in peripheral blood mononuclear cells of allogeneic hematopoietic cell transplant patients
title_sort lower expression of notch components in peripheral blood mononuclear cells of allogeneic hematopoietic cell transplant patients
topic Notch
Chronic graft-versus-host-disease
Allogeneic hematopoietic cell transplant
Tolerance
url http://www.sciencedirect.com/science/article/pii/S2531137922000864
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