Regulatory T cells after organ transplantation: Where does their action take place?

Dijke, I. Esmé; Weimar, Willem; Baan, Carla C.

doi:10.1016/j.humimm.2008.05.006

Cited by 45 publications

(27 citation statements)

References 83 publications

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“…The findings by Lanio et al could be explained by an increased intragraft homing of Treg in order to control rejection. Indeed, the preferential site in order to control allograft rejection would logically be the graft itself [5], as has been demonstrated in an animal model, further suggesting that intragraft homing of these cells is important for long-term maintenance of tolerance [25]. In this light, our results in long-term stable heart recipients suggest that this regulatory process is ongoing and perhaps responsible for good tolerance of the transplanted heart.…”

Section: Treg and Inkt Cells In Allograft Recipientssupporting

confidence: 61%

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Reduced levels of both circulating CD4+CD25+CD127low/neg and CD4+CD8neg invariant natural killer regulatory T cells in stable heart transplant recipients

Chen

Mohtize

Mattei

et al. 2010

Clinical and Experimental Immunology

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SummaryA cross-regulation between two regulatory T cell (Treg) subsets [CD4 + CD25 + and invariant natural killer (NK) T -iNK T] has been described to be important for allograft tolerance induction. However, few studies have evaluated these cellular subsets in stable recipients as correlates of favourable clinical outcome after heart transplantation. Treg and iNK T cell levels were assayed by flow cytometry in peripheral blood samples from 44 heart transplant recipients at a 2-year interval in 38 patients, and related to clinical outcome. Multiparameter flow cytometry used CD4/CD25/CD127 labelling to best identify Treg, and a standard CD3/CD4/CD8/Va24/Vb11 labelling strategy to appreciate the proportions of iNK T cells. Both subtypes of potentially tolerogenic cells were found to be decreased in stable heart transplant recipients, with similar or further decreased levels after 2 years. Interestingly, the patient who presented with several rejection-suggesting incidents over this period displayed a greater than twofold increase of both cell subsets. These results suggest that CD4 + CD25 + CD127 low/neg Treg and iNK T cells could be involved in the local control of organ rejection, by modulating immune responses in situ, in clinically stable patients. The measurement of these cell subsets in peripheral blood could be useful for non-invasive monitoring of heart transplant recipients, especially in the growing context of tolerance-induction trials.

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Section: Treg and Inkt Cells In Allograft Recipientssupporting

confidence: 61%

“…Regulatory T cells (Treg) play a major role in the control of immune responses. Multiple populations of such cells with different imunophenotypes and mechanisms of action have been identified [4,5]. Among them, the best characterized are naturally occurring CD4 + T cells strongly expressing the interleukin (IL)-2 receptor-a chain, CD25.…”

Section: Introductionmentioning

confidence: 99%

Reduced levels of both circulating CD4+CD25+CD127low/neg and CD4+CD8neg invariant natural killer regulatory T cells in stable heart transplant recipients

Chen

Mohtize

Mattei

et al. 2010

Clinical and Experimental Immunology

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“…Increased expression of cytokine-related genes (IL-4, IL-5, IL-13 and IFN-␥) and costimulatory and inhibitory genes (4-1BB, Icos and PD-1) was seen, with diminished expression of IL-1, IL-6, ICAM-1, Light, OX40, JAK-1, Fos and Jun. In addition to enhanced expression of genes associated with Treg populations (Foxp3, GITR, CTLA-4 and IL-10), we also observed increased expression of chemokine receptor CCR4, a molecule reported to play a key role in attraction of regulatory T cell populations to transplanted organs and/or secondary lymph organs [9,13] (Fig. 2).…”

Section: Increased Graft Survival In Cd200 Tg Mice Is Associated Withmentioning

confidence: 68%

CCR4 dependent migration of Foxp3+ Treg cells to skin grafts and draining lymph nodes is implicated in enhanced graft survival in CD200tg recipients

et al. 2011

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“…172 Treg cells are often considered the homeostatic controllers/suppressors of inflammation and immune reactions, partly through their expression of anti-inflammatory cytokines such as IL-10 and TGF-␤. 172 As such, they have also been suggested as potential role players in rejection post-transplant (reviewed elsewhere 173 ).…”

Section: T Cellsmentioning

confidence: 99%

Inflammation in Myocardial Diseases

Marchant

Boyd

Lin

et al. 2012

Circulation Research

246

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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Regulatory T cells after organ transplantation: Where does their action take place?

Cited by 45 publications

References 83 publications

Reduced levels of both circulating CD4+CD25+CD127low/neg and CD4+CD8neg invariant natural killer regulatory T cells in stable heart transplant recipients

Reduced levels of both circulating CD4+CD25+CD127low/neg and CD4+CD8neg invariant natural killer regulatory T cells in stable heart transplant recipients

CCR4 dependent migration of Foxp3+ Treg cells to skin grafts and draining lymph nodes is implicated in enhanced graft survival in CD200tg recipients

Inflammation in Myocardial Diseases

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