In this section
@article{Maher:2024:10.1172/jci.insight.173738,
author = {Maher, A and Aristodemou, A and Giang, N and Tanaka, Y and Bangham, C and Taylor, G and Dominguez-Villar, M},
doi = {10.1172/jci.insight.173738},
journal = {Journal of Clinical Investigation Insight},
title = {HTLV-1 induces an inflammatory CD4+CD8+ T cell population in HTLV-1-associated myelopathy},
url = {http://dx.doi.org/10.1172/jci.insight.173738},
volume = {9},
year = {2024}
}
TY - JOUR
AB - Human T cell leukemia virus type 1 (HTLV-1) is a retrovirus with preferential CD4+ T cell tropism that causes a range of conditions spanning from asymptomatic infection to adult T-cell leukemia and HTLV-1-associated myelopathy (HAM), an inflammatory disease of the CNS. The mechanisms by which HTLV-1 induces HAM are poorly understood. By directly examining the ex vivo phenotype and function of T cells from asymptomatic carriers and patients with HAM, we show that patients with HAM have a higher frequency of CD4+CD8+ double positive (DP) T cells, which are infected with HTLV-1 at higher rates than CD4+ T cells. Displaying both helper and cytotoxic phenotypes, these DP T cells are highly pro-inflammatory and contain high frequencies of HTLV-1-specific cells. Mechanistically, we demonstrate that DP T cells arise by direct HTLV-1 infection of CD4+ and CD8+ T cells. High levels of CD49d and CXCR3 expression suggest that DP T cells possess the ability to migrate to the CNS, and when co-cultured with astrocytes, DP T cells induce proinflammatory astrocytes that express high levels of CXCL10, IFN-, and IL-6. These results demonstrate the potential of DP T cells to directly contribute to CNS pathology.
AU - Maher,A
AU - Aristodemou,A
AU - Giang,N
AU - Tanaka,Y
AU - Bangham,C
AU - Taylor,G
AU - Dominguez-Villar,M
DO - 10.1172/jci.insight.173738
PY - 2024///
SN - 0021-9738
TI - HTLV-1 induces an inflammatory CD4+CD8+ T cell population in HTLV-1-associated myelopathy
T2 - Journal of Clinical Investigation Insight
UR - http://dx.doi.org/10.1172/jci.insight.173738
UR - https://insight.jci.org/articles/view/173738
VL - 9
ER -