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Competition but not cross-competition controls T cell proliferation in transplant patients following cytomegalovirus reactivation

ABSTRACT: Competition but not cross-competition controls T cell proliferation in transplant patients following cytomegalovirus reactivation

PROVIDER: PRJNA705213 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13798400.fastq.gz	Fastqsanger.gz
	SRR13798500.fastq.gz	Fastqsanger.gz
	SRR13798600.fastq.gz	Fastqsanger.gz
	SRR13798700.fastq.gz	Fastqsanger.gz
	SRR13798800.fastq.gz	Fastqsanger.gz

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Competition but not cross-competition controls T cell proliferation in transplant patients following cytomegalovirus reactivation

Project description:Competition between antigen-specific T cells for peptide:MHC (p:MHC) complexes shapes the ensuing T cell response. T cells also compete for access to antigen presenting cells (APCs), which results in competition between T cells of different antigen specificities and is referred to as cross-competition. When both mechanisms are in place, a memory T cell population specific for just a single epitope can effectively limit de novo antigen-specific T cell responses. Whether human cytomegalovirus (CMV)-specific T cell responses prevent other de novo T cell responses is unknown, but of interest in a transplant context as well as the development of CMV-based vaccines. We assessed the extent of T cell competition and cross-competition in a cohort of non-myeloablative hematopoietic stem cell transplant (nmHSCT) patients. In our cohort, HSCT donors and recipients were CMV-seronegative and -positive, respectively, thus providing genetically distinct memory and naïve T cell populations. We used single-cell transcriptomics to track donor versus recipient-derived T cell clones. We found that recipient-derived CMV-specific memory T cells outcompeted donor-derived responses of identical specificity; however, expansion of other donor-derived T cell clones still occurred averaging 24 rounds of cell division. The transcriptional programs between expanding donor and recipient-derived cells were largely congruent and consistent with an effector T cell response. Our data further indicated that the composition of the T cell compartment changed due to expanding and contracting clones in the first 90 days post-nmHSCT. Overall, our data suggest that CMV-specific memory T cells compete for p:MHC but not APC access during CMV reactivation.

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Profiling the blood compartment of Hematopoietic Stem Cell Transplant patients during Human Cytomegalovirus reactivation

Project description:Human cytomegalovirus (HCMV) reactivation is a leading infectious cause of morbidity and mortality in hematopoietic stem cell transplantation (HSCT) patients. HCMV reactivation is characterized by detection of viral DNA in the blood (DNAemia), however, the role of the blood compartment during HCMV reactivation is not well characterized. Using powerful molecular tools, we characterized HCMV infection in Peripheral Blood Mononuclear Cells (PBMCs) during DNAemia in HCMV reactivating HSCT patients. Surprisingly we found that all PBMC populations harbored extremely low levels of viral DNA and extremely low levels of viral transcripts. Remarkably, the viral transcripts detected in these samples were mainly immediate early genes indicating that these cells do not go through a full productive cycle. Analysis of the cellular transcriptome revealed characteristic transcriptional changes in high DNAemic samples implying the development of HCMV-specific T cells and inhibition of regulatory T cell function. Overall, our data indicate that DNAemia in HCMV reactivating HSCT patients is associated with distinct immune signatures but is not necessarily accompanied by substantial infection of PBMCs, and that PBMCs are not productively infected. These findings are important for understanding the role of the blood compartment in progression and control of HCMV during reactivation.

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