Primary cutaneous CD8+ and CD56+ T-cell lymphomas express HLA-G and killer-cell inhibitory ligand, ILT2

Abstract Primary cutaneous lymphomas constitute a spectrum of diseases characterized by a clonal accumulation of lymphocytes in the skin. Cutaneous T-cell lymphomas of the cytotoxic phenotype, including CD8+ and CD56+ lymphomas, are rare entities that have only been recently recognized and characterized. These lymphomas often show an aggressive clinical course. We investigated the expression of human leukocyte antigen G (HLA-G) and interleukin 10 (IL-10) in conjunction with expression of HLA-G killer-cell inhibitory receptor ligand immunoglobulin-like transcript 2 (ILT2) in 3 CD56+CD4+ and 4 CD8+ cutaneous T-cell lymphomas. HLA-G expression was detected in 2 of 3 lymphomas of the CD56+CD4+ type and in all lymphomas of CD8+ type. It is of note that CD56+CD4+ lymphomas displayed stronger HLA-G reactivity. The expression of IL-10 matched the expression of HLA-G. Together with the expression of IL-10, HLA-G might be one of the factors accounting for the evasion of immunosurveillance, thus contributing to aggressive phenotype of these lymphoma entities.

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Duvelisib as bridge to allotransplantation in refractory peripheral T-cell lymphoma with T-follicular helper phenotype: case report

Tumori Journal ◽

10.1177/03008916211027219 ◽

2021 ◽

pp. 030089162110272

Author(s):

Ginevra Lolli ◽

Beatrice Casadei ◽

Cinzia Pellegrini ◽

Lisa Argnani ◽

Federica Cocito ◽

...

Keyword(s):

Case Report ◽

T Cell ◽

Human Leukocyte ◽

Complete Response ◽

Unrelated Donor ◽

Phosphatidylinositol 3 Kinase ◽

Leukocyte Antigen ◽

Follicular Helper ◽

T Cell Lymphomas ◽

T Cell Malignancies

Objective: Peripheral T-cell lymphomas (PTCLs) are a group of heterogeneous T-cell malignancies representing 5%–10% of aggressive lymphomas. The prognosis is poor for patients with relapsed/refractory (R/R) disease, with a median overall survival of less than 6 months and no standardized treatments. We discuss the role of the phosphatidylinositol 3-kinase (PI3K) γδ inhibitor duvelisib as bridge to allotransplantation in a patient with R/R PTCL. Methods: Case report. Results: A 55-year-old woman diagnosed with relapsed nodal PTCL with T-follicular helper phenotype received PI3K γδ inhibitor duvelisib in the context of the phase II PRIMO clinical trial. After two cycles at a dose of 75 mg twice daily, the patient achieved complete response (CR), which was subsequently consolidated with human leukocyte antigen fully matched unrelated donor allotransplantation. No major toxicities were recorded during the duvelisib treatment period or during hospitalization for allotransplantation. At the latest follow-up, the patient was alive and still in CR 10 months posttransplant. Conclusions: Duvelisib should be further explored as a bridge to allotransplantation in patients with R/R PTCL, given the success and low toxicity in our patient.

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Haploidentical hematopoietic transplantation for the cure of leukemia: from its biology to clinical translation

Blood ◽

10.1182/blood-2016-07-730564 ◽

2016 ◽

Vol 128 (23) ◽

pp. 2616-2623 ◽

Cited By ~ 37

Author(s):

Antonella Mancusi ◽

Loredana Ruggeri ◽

Andrea Velardi

Keyword(s):

T Cell ◽

Ex Vivo ◽

Killer Cell ◽

Human Leukocyte ◽

Leukocyte Antigen ◽

Graft Versus Host ◽

Haploidentical Transplantation ◽

Hematopoietic Transplantation ◽

Human Leukocyte Antigen Haplotype ◽

Mother To Child

Abstract The present review describes the biology of human leukocyte antigen haplotype mismatched (“haploidentical”) transplantation, its translation to clinical practice to cure leukemia, and the results of current transplantation protocols. The 1990s saw what had been major drawbacks of haploidentical transplantation, ie, very strong host-versus-graft and graft-versus-host alloresponses, which led respectively to rejection and graft-versus-host disease (GVHD), being overcome through transplantation of a “mega-dose” of T cell–depleted peripheral blood hematopoietic progenitor cells and no posttransplant pharmacologic immunosuppression. The absence of posttransplant immunosuppression was an opportunity to discover natural killer cell alloreactions that eradicated acute myeloid leukemia and improved survival. Furthermore, it also unveiled the benefits of transplantation from mother donors, a likely consequence of the mother-to-child interaction during pregnancy. More recent transplantation protocols use unmanipulated (without ex vivo T-cell depletion) haploidentical grafts combined with enhanced posttransplant immunosuppression to help prevent GVHD. Unmanipulated grafts substantially extended the use of haploidentical transplantation with results than even rival those of matched hematopoietic transplantation. In T cell–depleted haploidentical transplantation, recent advances were made by the adoptive transfer of regulatory and conventional T cells.

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