Signaling of endothelial cytoprotection in transplantation

Charreau, Béatrice

doi:10.1016/j.humimm.2012.07.012

Cited by 9 publications

(7 citation statements)

References 103 publications

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“…In addition, humoral responses within intragraft de novo lymphoid tissue may target a more diverse antigenic repertoire, including pathogens, auto-antigens, and molecules involved in allograft accommodation. [32][33][34] The results of this study do not exclude the possibility that, in addition to providing optimal protective immunity against respiratory pathogens at local tissue sites, 35,36 de novo lymphoid tissue after LTx may play a regulatory role in lung graft tolerance.…”

Section: Discussioncontrasting

confidence: 58%

Association of Local Intrapulmonary Production of Antibodies Specific to Donor Major Histocompatibility Complex Class I With the Progression of Chronic Rejection of Lung Allografts

et al. 2017

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Section: Discussioncontrasting

confidence: 58%

Association of Local Intrapulmonary Production of Antibodies Specific to Donor Major Histocompatibility Complex Class I With the Progression of Chronic Rejection of Lung Allografts

et al. 2017

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“…However, there are some antibodies (class-and titer-dependent) that may help with allograft accommodation. 36 Future studies should determine the balance of antibodies with regard to titer and class as well as molecular mechanisms that determine overall allograft outcomes.…”

Section: Mechanisms Of Amrmentioning

confidence: 99%

Antibody-mediated rejection of the lung: A consensus report of the International Society for Heart and Lung Transplantation

Levine

Glanville

Aboyoun

et al. 2016

The Journal of Heart and Lung Transplantation

366

351

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Antibody-mediated rejection (AMR) is a recognized cause of allograft dysfunction in lung transplant recipients. Unlike AMR in other solid-organ transplant recipients, there are no standardized diagnostic criteria or an agreed-upon definition. Hence, a working group was created by the International Society for Heart and Lung Transplantation with the aim of determining criteria for pulmonary AMR and establishing a definition. Diagnostic criteria and a working consensus definition were established. Key diagnostic criteria include the presence of antibodies directed toward donor human leukocyte antigens and characteristic lung histology with or without evidence of complement 4d within the graft. Exclusion of other causes of allograft dysfunction increases confidence in the diagnosis but is not essential. Pulmonary AMR may be clinical (allograft dysfunction which can be asymptomatic) or sub-clinical (normal allograft function). This consensus definition will have clinical, therapeutic and research implications.

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“…188 Still, there are other antibodies (class-and titer-dependent) that may promote allograft accommodation. 189 Although antibody-mediated rejection (AMR) is a recognized clinical entity in renal and cardiac transplantation, with well-established diagnostic criteria, 190,191 AMR and its significance after lung transplantation remains a topic of controversy. 192,193 AMR is discussed in detail elsewhere within this issue.…”

Section: Humoral Immunity and Cladmentioning

confidence: 99%

Chronic Lung Allograft Dysfunction: Evolving Concepts and Therapies

Amubieya

Ramsey

Derhovanessian

et al. 2018

Semin Respir Crit Care Med

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Lung transplantation has become an established therapeutic option for a variety of end-stage lung diseases. Technical advances in graft procurement, implantation, perioperative care, immunosuppression, and posttransplant medical management have led to significant improvements in 1-year survival, but outcomes after the first year have improved minimally over the last two decades. The main limitation to better long-term survival after lung transplantation is chronic lung allograft dysfunction (CLAD). CLAD also impairs quality of life and increases the costs of medical care. Our understanding of CLAD manifestations, risk factors, and mechanisms is rapidly evolving. Recognition of different CLAD phenotypes (e.g., bronchiolitis obliterans syndrome and restrictive allograft syndrome) and the unique pathogenic mechanisms will be important for developing novel therapies. In addition to alloimmune-mediated rejection, we now recognize the importance of alloimmune-independent mechanisms of injury to the allograft. CLAD is the consequence of dysregulated repair of allograft injury. Unfortunately, currently available therapies for CLAD are usually not effective. However, the advances in knowledge, reviewed in this manuscript, should lead to novel strategies for CLAD prevention and treatment, as well as improvement in long-term outcomes after lung transplantation. We provide an overview of the evolving terminology related to CLAD, its varying clinical phenotypes and their diagnosis, natural history, pathogenesis, and potential treatments.

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Signaling of endothelial cytoprotection in transplantation

Cited by 9 publications

References 103 publications

Association of Local Intrapulmonary Production of Antibodies Specific to Donor Major Histocompatibility Complex Class I With the Progression of Chronic Rejection of Lung Allografts

Association of Local Intrapulmonary Production of Antibodies Specific to Donor Major Histocompatibility Complex Class I With the Progression of Chronic Rejection of Lung Allografts

Antibody-mediated rejection of the lung: A consensus report of the International Society for Heart and Lung Transplantation

Chronic Lung Allograft Dysfunction: Evolving Concepts and Therapies

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