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doi:10.6002/ect.2014.0049

Cited by 2 publications

(2 citation statements)

References 32 publications

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“…Notably, we demonstrated significant increases in absolute numbers of B lymphocytes in TCMR biopsies (Figure 2B), but not in AMR biopsies (Figure 3B). Although an unexpected result given the role of B lymphocyte lineage cells (plasma cells) in antibody production, these findings are in fact consistent with previous reports of B lymphocyte infiltration significantly associating with TCMR, but not with AMR (32, 33). These analogous findings from these earlier IHC-based studies further confirm the efficiency and integrity of our multi-color flow cytometric approach.…”

Section: Discussionsupporting

confidence: 91%

Specialized Roles of Human Natural Killer Cell Subsets in Kidney Transplant Rejection

et al. 2019

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Background: Human natural killer (NK) cells are key functional players in kidney transplant rejection. However, the respective contributions of the two functionally distinct human NK cell subsets (CD56 bright cytokine-producing vs. CD56 dim cytotoxic effector) in episodes of allograft rejection remain uncertain, with current immunohistochemical methods unable to differentiate these discrete populations. We report the outcomes of an innovative multi-color flow cytometric-based approach to unequivocally define and evaluate NK cell subsets in human kidney allograft rejection. Methods: We extracted renal lymphocytes from human kidney transplant biopsies. NK cell subsets were identified, enumerated, and phenotyped by multi-color flow cytometry. Dissociation supernatants were harvested and levels of soluble proteins were determined using a multiplex bead-based assay. Results were correlated with the histopathological patterns in biopsies—no rejection, borderline cellular rejection, T cell-mediated rejection (TCMR), and antibody-mediated rejection (AMR). Results: Absolute numbers of only CD56 bright NK cells were significantly elevated in TCMR biopsies. In contrast, both CD56 bright and CD56 dim NK cell numbers were significantly increased in biopsies with histopathological evidence of AMR. Notably, expression of the activation marker CD69 was only significantly elevated on CD56 dim NK cells in AMR biopsies compared with no rejection biopsies, indicative of a pathogenic phenotype for this cytotoxic NK cell subset. In line with this, we detected significantly elevated levels of cytotoxic effector molecules (perforin, granzyme A, and granulysin) in the dissociation supernatants of biopsies with a histopathological pattern of AMR. Conclusions: Our results indicate that human NK cell subsets are differentially recruited and activated during distinct types of rejection, suggestive of specialized functional roles.

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Section: Discussionsupporting

confidence: 91%

Specialized Roles of Human Natural Killer Cell Subsets in Kidney Transplant Rejection

et al. 2019

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“…Carpio et al. ( 47 ) evaluated B-cell expression patterns and association with function and survival in dysfunctional kidney allografts. The patients were evaluated in 3 groups according to the Banff classification: no rejection (40 patients), TCMR (50 patients), and ABMR (20 patients).…”

Section: Allograft Inflammation Activates and Stimulates Infiltration Of Immune Cellsmentioning

confidence: 99%

The Impact of Inflammation on the Immune Responses to Transplantation: Tolerance or Rejection?

Ravindranath

Hilali²,

Filippone

2021

Front. Immunol.

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Transplantation (Tx) remains the optimal therapy for end-stage disease (ESD) of various solid organs. Although alloimmune events remain the leading cause of long-term allograft loss, many patients develop innate and adaptive immune responses leading to graft tolerance. The focus of this review is to provide an overview of selected aspects of the effects of inflammation on this delicate balance following solid organ transplantation. Initially, we discuss the inflammatory mediators detectable in an ESD patient. Then, the specific inflammatory mediators found post-Tx are elucidated. We examine the reciprocal relationship between donor-derived passenger leukocytes (PLs) and those of the recipient, with additional emphasis on extracellular vesicles, specifically exosomes, and we examine their role in determining the balance between tolerance and rejection. The concept of recipient antigen-presenting cell “cross-dressing” by donor exosomes is detailed. Immunological consequences of the changes undergone by cell surface antigens, including HLA molecules in donor and host immune cells activated by proinflammatory cytokines, are examined. Inflammation-mediated donor endothelial cell (EC) activation is discussed along with the effect of donor-recipient EC chimerism. Finally, as an example of a specific inflammatory mediator, a detailed analysis is provided on the dynamic role of Interleukin-6 (IL-6) and its receptor post-Tx, especially given the potential for therapeutic interdiction of this axis with monoclonal antibodies. We aim to provide a holistic as well as a reductionist perspective of the inflammation-impacted immune events that precede and follow Tx. The objective is to differentiate tolerogenic inflammation from that enhancing rejection, for potential therapeutic modifications. (Words 247).

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Cited by 2 publications

References 32 publications

Specialized Roles of Human Natural Killer Cell Subsets in Kidney Transplant Rejection

Specialized Roles of Human Natural Killer Cell Subsets in Kidney Transplant Rejection

The Impact of Inflammation on the Immune Responses to Transplantation: Tolerance or Rejection?

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