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| Content Provider | PubMed Central |
|---|---|
| Author | Stuller, Kathleen A. Cush, Stephanie S. Flaño, Emilio |
| Abstract | The direct effector mechanisms of CD4 T cells during γ-herpesvirus 68 (γHV68)-persistent infection are less well understood than those of their CD8 T cell counterparts, although there is substantial evidence that CD4 T cells are critical for the control of persistent γ-herpesvirus infection. Our results show that in γHV68-persistently infected mice, CD4 T cells are not cytokine polyfunctional, but there is a division of labor in the CD4 T cell compartment in which CD4 T cells polarize toward two distinct populations with different effector functions: IFN-γ producers and CD107+ cytolytic effectors. These two CD4 T cell effector populations degranulate and produce IFN-γ during steady state without need for exogenous antigenic restimulation, which is fundamentally different from that observed with γHV68-specific CD8 T cells. By using anti–IFN-γ Ab depletions and IFN-γ–deficient mice, we show that CD4 T cell-mediated cytotoxicity in vivo is not dependent on IFN-γ activity. In addition, our data show that purified CD4 T cells isolated from γHV68-latently infected mice have the capacity to inhibit γHV68 reactivation from latency. Our results support the concept that CD4 T cells are critical effectors for the control of γ-herpesvirus latent infection, and they mediate this effect by two independent mechanisms: IFN-γ production and cytotoxicity. |
| Related Links | http://dx.doi.org/10.4049/jimmunol.0902935 |
| Ending Page | 3856 |
| Page Count | 7 |
| Starting Page | 3850 |
| File Format | |
| ISSN | 00221767 |
| e-ISSN | 15506606 |
| Journal | Journal of immunology (Baltimore, Md. : 1950) |
| Issue Number | 7 |
| Volume Number | 184 |
| Language | English |
| Publisher Date | 2010-04-01 |
| Access Restriction | Open |
| Subject Keyword | Medicine(all) Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Immunology and Allergy Immunology |
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