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HTLV-1-infected thymic epithelial cells convey the virus to CD4 + T lymphocytes
- Source :
- Immunobiology. 222:1053-1063
- Publication Year :
- 2017
- Publisher :
- Elsevier BV, 2017.
-
Abstract
- The human T-lymphotropic virus type-1 (HTLV-1) is the causative agent of adult T cell leukemia/lymphoma (ATL) and HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). CD4+T cells are the main target of HTLV-1, but other cell types are known to be infected, including immature lymphocytes. Developing T cells undergo differentiation in the thymus, through migration and interaction with the thymic microenvironment, in particular with thymic epithelial cells (TEC) the major component of this three dimensional meshwork of non-lymphoid cells. Herein, we show that TEC express the receptors for HTLV-1 and can be infected by this virus through cell-cell contact and by cell-free virus suspensions. The expression of anti-apoptosis, chemokine and adhesion molecules genes are altered in HTLV-1-infected TEC, although gene expression of antigen presentation molecules remained unchanged. Furthermore, HTLV-1-infected TEC transmitted the virus to a CD4+ T cell line and to CD4+ T cells from healthy donors, during in vitro cellular co-cultures. Altogether, our data point to the possibility that the human thymic epithelial cells play a role in the establishment and progression of HTLV-1 infection, functioning as a reservoir and transmitting the virus to maturing CD4+ T lymphocytes, which in turn will cause disease in the periphery.
- Subjects :
- 0301 basic medicine
Chemokine
viruses
T cell
Immunology
Antigen presentation
T-cell leukemia
Virus
03 medical and health sciences
Interleukin 21
0302 clinical medicine
immune system diseases
hemic and lymphatic diseases
Tropical spastic paraparesis
medicine
Immunology and Allergy
Cytotoxic T cell
biology
virus diseases
Hematology
medicine.disease
Virology
Molecular biology
030104 developmental biology
medicine.anatomical_structure
030220 oncology & carcinogenesis
biology.protein
Subjects
Details
- ISSN :
- 01712985
- Volume :
- 222
- Database :
- OpenAIRE
- Journal :
- Immunobiology
- Accession number :
- edsair.doi...........f31be89386d1559aba6539d4ffd98fb5
- Full Text :
- https://doi.org/10.1016/j.imbio.2017.08.001