HSV-1-infected oral epithelial cells are targets for natural killer cells
A mechanism of cell-mediated immunity was investigated to determine whether natural killer (NK) cells were able to lyse antigenically-altered epithelial cell targets. Using standard four-hour chromium-release assays, we tested human peripheral blood lymphocytes against autologous untreated epithelia...
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| Vydáno v: | Journal of dental research Ročník 66; číslo 3; s. 770 |
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| Hlavní autoři: | , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
United States
01.03.1987
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| Témata: | |
| ISSN: | 0022-0345 |
| On-line přístup: | Zjistit podrobnosti o přístupu |
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| Shrnutí: | A mechanism of cell-mediated immunity was investigated to determine whether natural killer (NK) cells were able to lyse antigenically-altered epithelial cell targets. Using standard four-hour chromium-release assays, we tested human peripheral blood lymphocytes against autologous untreated epithelial cells and autologous HSV-1-infected epithelial cells and calculated the percentage of lysis. With adherent cell-depleted peripheral blood, only epithelial cells infected with virus were lysed (p = 0.009). Evidence that NK cells were responsible for the lysis exists because: (1) peripheral blood lymphocytes were able to lyse allogeneic as well as autologous virus-infected cells; (2) when NK cells were depleted with the lysosomotropic drug L-leucine methyl ester, cytotoxicity against infected targets was abrogated; and (3) depletion of NK cells by the monoclonal antibody Leu-11b, plus complement, also eliminated cytotoxicity against virus-infected targets. Additional evidence suggests that lysis of targets does not involve antibody-dependent cellular cytotoxicity. These findings indicate that NK cells have the potential to perform a similar in vivo immunologic role in the oral cavity and initiate cell-mediated lysis of virus-infected epithelial cells. |
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| Bibliografie: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| ISSN: | 0022-0345 |
| DOI: | 10.1177/00220345870660031301 |