The time pattern of organ infiltration and distribution of natural killer cells and macrophages in the course of acute graft rejection after allogeneic heart transplantation in the rat

Dresske, Bettina; Zhu, Xiaofeng; Herwartz, C; Brötzmann, K.; Fändrich, F.

doi:10.1016/s0041-1345(97)00026-2

Cited by 15 publications

(7 citation statements)

References 5 publications

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“…160 Involvement of both natural killer (NK) cells, a class of cytotoxic lymphocytes, and macrophages during early phases posttransplant, as part of the nonadaptive/ innate immune response, has been demonstrated in in vivo studies. 177,178 In a rat heart transplant model, infiltration of recipient NK cells and macrophages can be observed as early as 3 hours posttransplant in the myocardial interstitial regions and allograft vessel endothelium; at 3 days post-transplant, a maximum number of NK cells and macrophage were found in the endo-, epi-, and myocardial portions of the wall of the transplanted heart. 177,178 This is typically followed by the infiltration of T-and B-cell populations in the endo-and subendomyocardial walls.…”

Section: Natural Killer Cells and Macrophagesmentioning

confidence: 99%

“…177,178 In a rat heart transplant model, infiltration of recipient NK cells and macrophages can be observed as early as 3 hours posttransplant in the myocardial interstitial regions and allograft vessel endothelium; at 3 days post-transplant, a maximum number of NK cells and macrophage were found in the endo-, epi-, and myocardial portions of the wall of the transplanted heart. 177,178 This is typically followed by the infiltration of T-and B-cell populations in the endo-and subendomyocardial walls. 177,178 In CD28 Ϫ/Ϫ mice heart transplant models (deficient of costimulatory signal; thought to be dependent on CD8ϩ T cell and NK cells-mediated effects to cause rejection), blockade of a NK cell-activating receptor (NKG2D) using anti-NKG2D monoclonal Ab prevented the occurrence of acute cardiac rejection.…”

Section: Natural Killer Cells and Macrophagesmentioning

confidence: 99%

“…177,178 This is typically followed by the infiltration of T-and B-cell populations in the endo-and subendomyocardial walls. 177,178 In CD28 Ϫ/Ϫ mice heart transplant models (deficient of costimulatory signal; thought to be dependent on CD8ϩ T cell and NK cells-mediated effects to cause rejection), blockade of a NK cell-activating receptor (NKG2D) using anti-NKG2D monoclonal Ab prevented the occurrence of acute cardiac rejection. 179 Based on this observation, it has been suggested that NK cells may mediate CD8ϩ T-cell proliferation, possibly via cytokine secretion or dendritic cell (DC) maturation promotion, and thereby contribute to the myocardial inflammation process, leading to acute cellular rejection.…”

Section: Natural Killer Cells and Macrophagesmentioning

confidence: 99%

See 2 more Smart Citations

Inflammation in Myocardial Diseases

Marchant

Boyd

Lin

et al. 2012

Circulation Research

247

165

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Inflammatory processes underlie a broad spectrum of conditions that injure the heart muscle and cause both structural and functional deficits. In this article, we address current knowledge regarding 4 common forms of myocardial inflammation: myocardial ischemia and reperfusion, sepsis, viral myocarditis, and immune rejection. Each of these pathological states has its own unique features in pathogenesis and disease evolution, but all reflect inflammatory mechanisms that are partially shared. From the point of injury to the mobilization of innate and adaptive immune responses and inflammatory amplification, the cellular and soluble mediators and mechanisms examined in this review will be discussed with a view that both beneficial and adverse consequences arise in these human conditions. (Circ Res. 2012;110:126-144.)

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Section: Natural Killer Cells and Macrophagesmentioning

confidence: 99%

Section: Natural Killer Cells and Macrophagesmentioning

confidence: 99%

Section: Natural Killer Cells and Macrophagesmentioning

confidence: 99%

See 1 more Smart Citation

Inflammation in Myocardial Diseases

Marchant

Boyd

Lin

et al. 2012

Circulation Research

247

165

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“…Indeed, in contradistinction to earlier studies, recent findings show that NK cells become activated early after organ transplantation and can contribute to the cell-mediated alloresponse and acute rejection process [21,22,33–35]. In the first few days after transplantation of cardiac allografts in rodents, the majority of infiltrating lymphocytes were found to be NK cells [36]. It is noteworthy that early NK cell activation and graft infiltration is only observed in recipients of allogeneic but not syngeneic organ transplants [37].…”

Section: Role In Acute Rejectionmentioning

confidence: 99%

Natural killer cells in rejection and tolerance of solid organ allografts

Bénichou¹,

Yamada²,

Aoyama³

et al. 2011

Current Opinion in Organ Transplantation

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Purpose of review A series of recent papers defy conventional wisdom by showing that NK cells exert a powerful and long lasting influence on the immune response to whole organ allografts. The early activation of NK cells following transplantation is associated with killing of allogeneic target cells and release of immunomodulatory chemokines and cytokines, which can contribute to either rejection or tolerance. Here, we review findings describing NK cell receptors, potential mediators and mechanisms underlying the dual influence of NK cells in solid organ transplantation. Findings New studies show that NK cells can discriminate between self and foreign tissues and play a key role in the initiation and regulation of adaptive immune responses after solid organ transplantation. Depending upon the types of NK cell receptors engaged and the nature of cytokines released, early NK cell activation can promote either acute rejection or tolerance. Summary Solid organ transplantation is associated with the early activation of NK cells, which are then licensed to kill allogeneic target cells directly or via ADCC and release various chemokines and immunomodulatory cytokines. Depending upon the nature of NK cell subsets activated and their ability to kill allogeneic target cells and release certain types of cytokines, NK cells can promote the activation/expansion of pro-inflammatory Th1 cells or regulatory Th2/Treg cells thus tilting the balance of alloimmunity towards rejection or tolerance. An in-depth understanding of these mechanisms will be necessary in order to design therapies targeting NK cells in human transplantation.

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“…In the first few days after allogeneic heart transplantation, the majority of infiltrating lymphocytes are NK cells. 3 In murine recipients of cardiac allografts, expression of the NK cell-activating receptor NKG2D and its ligands, including retinoic acid early inducible (RAE-1) and minor histocompatibility antigen H60, is upregulated from 3 to 5 days after transplantation. 4 Expression increases with time as rejection develops, and only a modest effect is seen in the recipients of syngeneic grafts, suggesting that this receptor–ligand interaction could have a role in stimulating rejection.…”

Section: Nk Cellsmentioning

confidence: 99%

Innate immunity and cardiac allograft rejection

Millington

Madsen

2010

Kidney International

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The development of immunosuppressive drugs to control adaptive immune responses has led to the success of heart transplantation as a therapy for end-stage heart failure. However, these agents are largely ineffective in suppressing components of the innate immune system. This distinction has gained clinical significance as mounting evidence now indicates that innate immune responses have important roles in the acute and chronic rejection of cardiac allografts including cardiac allograft vasculopathy (CAV). Whereas clinical interest in natural killer (NK) cells was once largely confined to the field of bone marrow transplantation, recent findings suggest that these cells can also participate in the acute rejection of cardiac allografts and in the development of CAV. Stimulation of Toll-like receptors (TLRs), another important component of innate immunity, by endogenous ligands released in response to ischemia/reperfusion is now known to cause an inflammatory milieu favorable to graft rejection. Finally, new data indicate that activation of complement is linked to acute rejection and CAV. In summary, the conventional wisdom that the innate immune system is of little importance in whole-organ transplantation is no longer tenable. The addition of strategies that target TLRs, NK cells, and complement will be necessary to prevent CAV completely and to eventually achieve long-term tolerance to cardiac allografts.

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The time pattern of organ infiltration and distribution of natural killer cells and macrophages in the course of acute graft rejection after allogeneic heart transplantation in the rat

Cited by 15 publications

References 5 publications

Inflammation in Myocardial Diseases

Inflammation in Myocardial Diseases

Natural killer cells in rejection and tolerance of solid organ allografts

Innate immunity and cardiac allograft rejection

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