T cells from HIV-1+ individuals have a defect in mounting an antigen specific response. HIV-1 Tat has been implicated as the causative agent of this immunosuppression. We have previously shown that HIV-1 Tat inhibits antigen specific proliferation of normal T cells in vitro by binding to the accessory molecule CD26, a dipeptidase expressed on the surface of activated T cells. We now demonstrate that the defective in vitro recall antigen response in HIV-1 infected individuals can be restored by the addition of soluble CD26, probably by serving as a decoy receptor for HIV-1 Tat. The restored response is comparable to that of an HIV-1- individual, suggesting that early in HIV infection there is a block in the memory cell response, rather than deletion of these cells.
T Schmitz, R Underwood, R Khiroya, W W Bachovchin, B T Huber
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International journal of molecular sciences | 2024 |
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CD26, let it cut or cut it down
ID Meester, S Korom, JV Damme, S Scharpé |
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The N-terminal Structure of HIV-1 Tat Is Required for Suppression of CD26-dependent T Cell Growth
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S Ansorge, J Langner |
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Dipeptidyl-Peptidase IV-beta, a Novel form of Cell-Surface-Expressed Protein with Dipeptidyl-Peptidase IV Activity
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