Disease relevance of HTLVR

• Up-regulation of the HTLV receptor, via signals transmitted through the IL-7 cytokine receptor as well as the TCR, is likely to contribute to the mother-to-infant transmission and spreading of HTLV-1 [1].
• The identification of CD4 as the primary receptor for HIV followed shortly after the discovery of the virus, but the HTLV receptor remained long elusive, until its recent identification as the GLUT1 glucose transporter [2].

High impact information on HTLVR

• Our identification of GLUT1 as the human T lymphotrophic virus (HTLV) receptor has enabled us to use tagged HTLV-receptor-binding domain fusion proteins to specifically monitor surface GLUT1 expression [3].
• The HTLV receptor is an early T-cell activation marker whose expression requires de novo protein synthesis [1].
• Neonatal, but not adult, lymphocytes proliferate in response to IL-7 and HTLV receptor expression is restricted to the former population [1].
• Thus, HTLV receptor expression appears to be an early marker of cell cycle entry [1].
• To determine whether HTLV receptor up-regulation specifically requires TCR-mediated signals or, alternatively, is dependent on more generalized cell cycle entry/proliferation signals, its expression was monitored in interleukin 7 (IL-7)-stimulated neonatal and adult T cells [1].

Biological context of HTLVR

• Assignment of the possible HTLV receptor gene to chromosome 17q21-q23 [4].
• Our results from the induced syncytium pattern of the somatic hybrid cell lines with different deletions indicated that the HTLV receptor gene may reside from q21 to q23 on the long arm of the human chromosome 17 [4].
• Binding resulted from bona fide interaction with the HTLV receptor as isolated SU subdomains specifically interfered with HTLV Env-mediated binding, cell fusion, and cell-free as well as cell-to-cell infection [5].

Anatomical context of HTLVR

• This induced surface expression of the HTLV receptor requires de novo protein synthesis and results in a wide distribution on the surface of activated lymphocytes [1].

Associations of HTLVR with chemical compounds

• Therefore, the HTLV receptor-binding domain (RBD) lies in the amino terminus of the SU, immediately upstream of a central immunodominant proline rich region (Env residues 180 to 205), that we show to be dispensible for receptor-binding and interference [5].

Other interactions of HTLVR

• These data show that NRP1 is involved in HTLV-1 and HTLV-2 entry, suggesting that the HTLV receptor has a multicomponent nature [6].

Analytical, diagnostic and therapeutic context of HTLVR

• Moreover, the distribution of the HTLV receptor is independent of TCR/CD3-capped membrane structures, as observed by confocal immunofluorescence microscopy [1].

References