| First Author | Harbour JC | Year | 2023 |
| Journal | Cell Rep | Volume | 42 |
| Issue | 5 | Pages | 112407 |
| PubMed ID | 37083328 | Mgi Jnum | J:349752 |
| Mgi Id | MGI:7491471 | Doi | 10.1016/j.celrep.2023.112407 |
| Citation | Harbour JC, et al. (2023) T helper 1 effector memory CD4(+) T cells protect the skin from poxvirus infection. Cell Rep 42(5):112407 |
| abstractText | Poxvirus infections of the skin are a recent emerging public health concern, yet the mechanisms that mediate protective immunity against these viral infections remain largely unknown. Here, we show that T helper 1 (Th1) memory CD4(+) T cells are necessary and sufficient to provide complete and broad protection against poxvirus skin infections, whereas memory CD8(+) T cells are dispensable. Core 2 O-glycan-synthesizing Th1 effector memory CD4(+) T cells rapidly infiltrate the poxvirus-infected skin microenvironment and produce interferon gamma (IFNgamma) in an antigen-dependent manner, causing global changes in gene expression to promote anti-viral immunity. Keratinocytes express IFN-stimulated genes, upregulate both major histocompatibility complex (MHC) class I and MHC class II antigen presentation in an IFNgamma-dependent manner, and require IFNgamma receptor (IFNgammaR) signaling and MHC class II expression for memory CD4(+) T cells to protect the skin from poxvirus infection. Thus, Th1 effector memory CD4(+) T cells exhibit potent anti-viral activity within the skin, and keratinocytes are the key targets of IFNgamma necessary for preventing poxvirus infection of the epidermis. |
