2020
DOI: 10.1111/tri.13706
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Abstract: Over the last two decades, an additional and important role for B cells has been established in immune regulation. Preclinical studies demonstrate that regulatory B cells (Breg) can prolong allograft survival in animal models and induce regulatory T cells. Operationally tolerant human kidney transplant recipients demonstrate B-cell-associated gene signatures of immune tolerance, and novel therapeutic agents can induce Bregs in phase I clinical trials in transplantation. Our rapidly expanding appreciation of th… Show more

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Cited by 11 publications
(8 citation statements)
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“…FMT responders also exhibited higher fold changes in frequency of tolerogenic regulatory B cell populations and IL-4 producing CD4 T cells across all time points compared to the non-responder. These findings concur with evidence which demonstrates the protective capacity of immunosuppressive Bregs in the prevention of allograft rejection in renal, liver and lung transplantation recipients and in the development of graft-versus-host disease in stem cell recipients, and with increased frequencies of CD4 +ve T cells in the colons of FMT-treated mice, respectively [72,73]. Our findings suggest that, in addition to glatiramer acetate, which is known to stimulate functional Bregs [74], IgG1 Fc N-glycopeptides with bisected and non-bisected monogalactosylated and monosiaylated glycans without core fucose may help induce this Breg tolerogenic phenotype, whereas certain taxa such as Acidaminococcaceae, Phascolartobacterium and Fastiosipila, in addition to the fecal bile acids 3-alpha-Hydroxy-7 ketolithocholic acid and chenodeoxycholic acid, may negatively regulate Bregs.…”
Section: Discussionsupporting
confidence: 89%
“…FMT responders also exhibited higher fold changes in frequency of tolerogenic regulatory B cell populations and IL-4 producing CD4 T cells across all time points compared to the non-responder. These findings concur with evidence which demonstrates the protective capacity of immunosuppressive Bregs in the prevention of allograft rejection in renal, liver and lung transplantation recipients and in the development of graft-versus-host disease in stem cell recipients, and with increased frequencies of CD4 +ve T cells in the colons of FMT-treated mice, respectively [72,73]. Our findings suggest that, in addition to glatiramer acetate, which is known to stimulate functional Bregs [74], IgG1 Fc N-glycopeptides with bisected and non-bisected monogalactosylated and monosiaylated glycans without core fucose may help induce this Breg tolerogenic phenotype, whereas certain taxa such as Acidaminococcaceae, Phascolartobacterium and Fastiosipila, in addition to the fecal bile acids 3-alpha-Hydroxy-7 ketolithocholic acid and chenodeoxycholic acid, may negatively regulate Bregs.…”
Section: Discussionsupporting
confidence: 89%
“…The primary endpoint was chosen based on other studies of tolerance induction and included: (1) the primary efficacy endpoint requested by the European Medicines Agency, for example, no biopsy-proven acute rejection (>Banff borderline), graft loss, graft dysfunction with an estimated glomerular filtration rate (eGFR)<30 mL/min, or death at year 1, together with the absence of harmful donor-specific HLA antibodies, (2) the achievement of the desired immunosuppression reduction and (3) a phenotype that is specifically found in operational tolerance, that is, the induction of graft-protective transitional CD24 hi CD38 hi B lymphocytes (ie, Breg) 12–19. The aim is to develop a new immunosuppressant to improve efficacy and safety outcomes of well-established immunosuppressive regimens, and to introduce a new treatment approach such as tolerance induction and exclusion of maintenance therapy to replace well-established regimens.…”
Section: Methods and Analysismentioning
confidence: 99%
“…The allograft function was normal, and, as the patients showed unmodified levels of Tregs compared to pretransplant and pretreatment levels, the effectiveness of the treatment could be associated with the tolerogenic capacity of Bregs. Other therapeutic strategies targeting molecular regulators of Breg function, such as TIM-1, histone deacetylase, and the STAT3 network pathway, can have meaningful impact in inducing humoral-mediated immune suppression in tolerant allograft recipients ( 219 ).…”
Section: Therapeutic Strategies To Improve Immune Cell Tolerancementioning
confidence: 99%