Impact of HLA type, age and chronic viral infection on peripheral T-cell receptor sharing between unrelated individuals

Impact of HLA type, age and chronic viral infection on peripheral T-cell receptor sharing between unrelated individuals post thumbnail image

The human adaptive immune system must generate extraordinary diversity to be able to respond to all possible pathogens. The T-cell repertoire derives this high diversity through somatic recombination of the T-cell receptor (TCR) locus, a random process that results in repertoires that are largely private to each individual. However, factors such as thymic selection and T-cell proliferation upon antigen exposure can affect TCR sharing among individuals.

By immunosequencing the TCRβ variable region of 426 healthy individuals, we find that, on average, fewer than 1% of TCRβ clones are shared between individuals, consistent with largely private TCRβ repertoires. However, we detect a significant correlation between increased HLA allele sharing and increased number of shared TCRβ clones, with each additional shared HLA allele contributing to an increase in ~0.01% of the total shared TCRβ clones, supporting a key role for HLA type in shaping the immune repertoire.

Surprisingly, we find that shared antigen exposure to CMV leads to fewer shared TCRβ clones, even after controlling for HLA, indicative of a largely private response to major viral antigenic exposure. Consistent with this hypothesis, we find that increased age is correlated with decreased overall TCRβ clone sharing, indicating that the pattern of private TCRβ clonal expansion is a general feature of the T-cell response to other infectious antigens as well.

However, increased age also correlates with increased sharing among the lowest frequency clones, consistent with decreased repertoire diversity in older individuals. Together, all of these factors contribute to shaping the TCRβ repertoire, and understanding their interplay has important implications for the use of T cells for therapeutics and diagnostics.

 Impact of HLA type, age and chronic viral infection on peripheral T-cell receptor sharing between unrelated individuals

Successful treatment of refractory retroperitoneal Epstein-Barr virus-positive diffuse large B-cell lymphoma with secondary hemophagocytic syndrome by sequential combination regimen of PD-1 blockade and chimeric antigen receptor T cells: a case report

Epstein-Barr virus (EBV) is convincingly contributed to the development of several types of lymphomas such as NK/T cell lymphoma, Burkitt lymphoma, plasmablastic lymphoma, and diffuse large B cell lymphoma (DLBCL). Herein, we reported an atypical case of EBV-positive DLBCL in an immunocompetent young male patient who presented with epistaxis due to hypergammaglobulinemia.

2-Deoxy-2-[fluorine-8] fluoro-D-glucose PET/computed tomography showed multiple highly metabolic retroperitoneal tissue masses with the involvement of bilateral adrenal gland. Ultrasonography-guided biopsy revealed a significant number of lymphocytes and plasma-like cells that are immunopositive for plasma-cell markers and partly positive for pan-B cell markers.

The Ki-67 proliferation index was 20%. The extensive distribution of EBV-encoded small RNAs was confirmed by in-situ hybridization. Due to atypical/overlapping pathological characteristics, it was initially misdiagnosed as extramedullary plasmacytoma and treated with two cycles of bortezomib, lenalidomide, and dexamethasone.

Disease progression occurred and pathology consultation for the retroperitoneal biopsies modified the diagnosis to EBV-positive DLBCL with plasma cell differentiation. The treatment was adjusted to etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, rituximab, and lenalidomide (R2-EPOCH), but no response was observed after three cycles of treatment and he developed hemophagocytic syndrome during treatment.

A monotherapy of anti-programmed cell death-1 (PD-1) treatment with tiririzumab was administered, successfully controlling hemophagocytic syndrome and EBV infection. The response assessment was partial for EBV-positive DLBCL, subsequent anti-CD19 chimeric antigen receptor-T (CAR-T) cell therapy resulted in complete remission including lumps, immunoglobulins, and negative EBV-DNA 1.5 months later.

The present case study proved the possibility of PD-1 blockade in controlling EBV infection and associated hemophagocytic syndrome and offered an example of the combination of CAR-T therapy and PD-1 blockade for refractory EBV-positive DLBCL in clinic.

Chimeric antigen receptor Tcells (CARs) in cancer treatment

Cancer is one of the leading causes of death worldwide. Chemotherapy, radiation therapy, and stem cell transplantation were the main cancer treatment approaches for several years but due to their limited effectiveness, there was a constant search for new therapeutic approaches.

Cancer immunotherapy that utilizes and enhances the normal capacity of the patient’s immune system was used to fight against cancer. Genetically engineered T-cells that express chimeric antigen receptors (CARs) showed remarkable anti-tumor activity against hematologic malignancies and is now being investigated in a variety of solid tumors.

The use of this therapy in the last few years has been successful, achieving a great success in improving the quality of life and prolonging the survival time of patients with a reduction in remission rates. However, many challenges still need to be resolved in order for this technology to gain widespread adoption.

This review summarizes various experimental approaches towards the use of CAR T-cells in hematologic malignancies and solid tumors. <P> Conclusion: Finally, we address the challenges posed by CAR T-cells and discuss strategies for improving the performance of these T cells in fighting cancers.

Inhibition of MEK pathway enhances the antitumor efficacy of chimeric antigen receptor T cells against neuroblastoma

Disialoganglioside (GD2)-specific chimeric antigen receptor (CAR)-T cells (GD2-CAR-T cells) have been developed and tested in early clinical trials in patients with relapsed/refractory neuroblastoma. However, the effectiveness of immunotherapy using these cells is limited, and requires improvement. A combinatorial therapy with CAR-T cells and molecular targeted drugs could be a promising strategy to enhance the antitumor efficacy of CAR T-cell immunotherapy.

Here, we generated GD2-CAR-T cells via piggyBac transposon (PB)-based gene transfer (PB-GD2-CAR-T cells), and analyzed the combinatorial effect of these cells and a mitogen-activated protein kinase kinase (MEK) inhibitor in vitro and in vivo on neuroblastoma.

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Trametinib, a MEK inhibitor, ameliorated the killing efficacy of PB-GD2-CAR-T cells in vitro, whereas a combinatorial treatment of the two exhibited superior antitumor efficacy in a murine xenograft model compared to that of PB-GD2-CAR-T cell monotherapy, regardless of the mutation status of MAPK pathway in tumor cells. The results presented here provide new insights into the feasibility of combinatorial treatment with CAR-T cells and MEK inhibitors in patients with neuroblastoma.

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