Autor: |
de Souza, A. P. Duarte, de Freitas, D. Nascimento, Antuntes Fernandes, K. E., D'Avila da Cunha, M., Antunes Fernandes, J. L., Benetti Gassen, R., Fazolo, T., Pinto, L. A., Scotta, M., Mattiello, R., Pitrez, P. M., Bonorino, C., Stein, R. T. |
Předmět: |
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Zdroj: |
Clinical & Experimental Immunology; Feb2016, Vol. 183 Issue 2, p248-257, 10p, 1 Chart, 6 Graphs |
Abstrakt: |
Respiratory syncytial virus (RSV)-specific CD8+ T cell responses do not protect against reinfection. Activation of mammalian target of rapamycin (mTOR) impairs memory CD8+ T cell differentiation. Our hypothesis was that RSV inhibits the formation of CD8+ T cells memory responses through mTOR activation. To explore this, human and mouse T cells were used. RSV induced mTOR phosphorylation at Ser2448 in CD8 T cells. mTOR activation by RSV was completely inhibited using rapamycin. RSV-infected children presented higher mTOR gene expression on nasal washes comparing to children infected with metapneumovirus and rhinovirus. In addition, RSV-infected infants presented a higher frequency of CD8+ pmTORser2448+ T cells in nasal washes compared to RSV-negative infants. Rapamycin treatment increased the frequency of mouse CD8 RSV-M282-90 pentamer-positive T cells and the frequency of RSV-specific memory T cells precursors. These data demonstrate that RSV is activating mTOR directly in CD8 T cells, indicating a role for mTOR during the course of RSV infection. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
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