Data from HTLV-1 Viral Factor HBZ Induces CCR4 to Promote T-cell Migration and Proliferation

• DOI: 10.1158/0008-5472.c.6508860.v1
• Publication Date: 2023-03-31T22:23:17Z
• Authors: Kenji Sugata; Jun-ichirou Yasunaga; Haruka Kinosada; Yuichi Mitobe; Rie Furuta; Mohamed Mahgoub; Chiho Onishi; Kazutaka Nakashima; Koichi Ohshima; Masao Matsuoka
• Keywords: CCR4; Jurkat cells

<div>Abstract<p>Human T-cell leukemia virus type 1 (HTLV-1) causes adult leukemia-lymphoma (ATL) and other inflammatory diseases in infected individuals. However, a complete understanding of how HTLV-1 transforms T cells is lacking. Expression the chemokine receptor CCR4 on ATL HTLV-1–infected suggested hypothesis that may mediate features caused by HTLV-1. In this study, we show constitutively expressed bZIP factor (HBZ) encoded responsible for inducing its ability to promote proliferation migration. Ectopic expression HBZ was sufficient stimulate human mouse cells. Conversely, silencing cell lines inhibit expression. Mechanistic investigations showed induced GATA3 CD4<sup>+</sup> cells, thereby activating transcription from promoter. an established air pouch model ATL, observed transgenic mice (HBZ-Tg mice) migrated preferentially pouch, as compared with those nontransgenic mice. Migration HBZ-Tg inhibited treatment antagonist. Proliferating (Ki67<sup>+</sup>) were found express high levels CD103. Further, enhanced coordinate ligands CCL17 22 CD103 ligand E-cadherin. Consistent finding, clinical skin lesions frequently positive CCR4, CD103, Ki67. Taken together, our results activates augment their migration proliferation, two phenomena linked pathogenesis. <i>Cancer Res; 76(17); 5068–79. ©2016 AACR</i>.</p></div>