التفاصيل البيبلوغرافية
العنوان: |
Phenotypic and functional analysis of γδ T cells in the pathogenesis of human T-cell lymphotropic virus type 1 infection |
المؤلفون: |
Ruggieri, Matias, Ducasa, Nicolás, Juraske, Claudia, Polo, Virginia Gonzalez, Berini, Carolina, Quiroga, Maria Florencia, Christopoulos, Petros, Minguet, Susana, Biglione, Mirna, Schamel, Wolfgang W. |
المصدر: |
Frontiers in Immunology ; volume 13 ; ISSN 1664-3224 |
بيانات النشر: |
Frontiers Media SA |
سنة النشر: |
2022 |
المجموعة: |
Frontiers (Publisher - via CrossRef) |
مصطلحات موضوعية: |
Immunology, Immunology and Allergy |
الوصف: |
The human T-cell leukemia virus type 1 (HTLV-1) is the cause of serious malignant and inflammatory diseases, including adult T-cell leukemia and lymphoma and tropical spastic paraparesis. The potential protective role of γδ T cells in HTLV-1 infection remains unclear. Here, demonstrate that there is a decrease in the amount of Vγ9Vδ2 T cells in patients with HTLV-1, especially in those with HTLV-1 associated pathologies. This suggests that γδ T cells could be involved in controlling the virus. Indeed, we found that Vγ9Vδ2 T cells, expanded from non-infected individuals, can kill cells expressing the viral proteins HBZ and Tax and this phenotype is reversed in the presence of mevastatin. Cytotoxicity by Vγ9Vδ2 T cells was not associated with an increase of INF-γ production. In sharp contrast, killing by NK cells was reduced by Tax expression. Thus, our study provides initial evidence for a potential protective role of Vγ9Vδ2 T cells against HTLV-1 infection. Therapeutic exploitation of these insights is feasible with current technologies of T-cell therapies and could provide novel tools to prevent and treat HTLV-1-associated malignancies and neurologic complications. |
نوع الوثيقة: |
article in journal/newspaper |
اللغة: |
unknown |
DOI: |
10.3389/fimmu.2022.920888 |
DOI: |
10.3389/fimmu.2022.920888/full |
الإتاحة: |
https://doi.org/10.3389/fimmu.2022.920888Test |
حقوق: |
https://creativecommons.org/licenses/by/4.0Test/ |
رقم الانضمام: |
edsbas.196936A |
قاعدة البيانات: |
BASE |