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Eosinophils in Lung Allograft

ABSTRACT: Eosinophils in Lung Allograft

PROVIDER: PRJNA925858 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23152921_1.fastq.gz	Fastqsanger.gz
	SRR23152921_2.fastq.gz	Fastqsanger.gz
	SRR23152922_1.fastq.gz	Fastqsanger.gz
	SRR23152922_2.fastq.gz	Fastqsanger.gz
	SRR23152923_1.fastq.gz	Fastqsanger.gz

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Eosinophils Restrain Humoral Alloimmunity after Lung Transplantation [scRNA-seq]

Project description:While the function of many leukocytes in transplant biology has been well defined, the role of eosinophils is controversial and remains poorly explored. Conflicting data exist regarding eosinophils’ role in alloimmunity based on context and organ type. Due to their prevalence in the lung, and their defined role in other pulmonary pathology such as asthma, we set out to explore the role of eosinophils in the long-term maintenance of the lung allograft. We noted that depletion of eosinophils results in the generation of donor-specific antibodies. Eosinophil depletion increased memory B cell, plasma cell, and antibody secreting cell differentiation and resulted in de novo-generation of follicular germinal centers. Germinal center formation depended on the expansion of CD4+Foxp3-Bcl6+CXCR5+PD1+ T follicular helper cells (Tfh) which increase in number after eosinophil depletion. Mechanistically, we demonstrate that eosinophils prevent Tfh generation by acting as the dominant source of IFN-γ in an established lung allograft, thus facilitating Th1 rather than Tfh polarization of naïve CD4+ T cells. Our data thus describe a unique and previously unknown role for eosinophils in maintaining allograft tolerance and suggests that indiscriminate administration of eosinophil-lytic corticosteroids for treatment of acute cellular rejection may inadvertently promote humoral alloimmunity.

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Blocking hyaluronan synthesis alleviates acute lung allograft rejection.

Project description:Lung allograft rejection results in the accumulation of low molecular weight hyaluronic acid (LMW-HA), which further propagates inflammation and tissue injury. We have previously shown that therapeutic lymphangiogenesis in a murine model of lung allograft rejection reduced tissue LMW-HA and was associated with improved transplant outcomes. Herein we investigated the use of 4-Methylumbelliferone (4-MU), a known inhibitor of HA synthesis, to alleviate acute allograft rejection in a murine model of lung transplantation. We found that treating mice with 4-MU from day 20-30 post-transplant was sufficient to significantly improve outcomes, characterized by a reduction in T-cell mediated lung inflammation, LMW-HA content and improved pathology scores. In vitro, 4-MU directly attenuated activation, proliferation, and differentiation of naïve CD4+ T-cells into Th1 cells. As 4-MU has already been demonstrated to be safe for human use, we believe examining 4-MU for the treatment of acute lung allograft rejection may be of clinical significance.

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Eosinophils Restrain Humoral Alloimmunity after Lung Transplantation

Project description:Eosinophils Restrain Humoral Alloimmunity after Lung Transplantation

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