| First Author | Guo Y | Year | 2013 |
| Journal | Infect Immun | Volume | 81 |
| Issue | 10 | Pages | 3923-34 |
| PubMed ID | 23918785 | Mgi Jnum | J:200593 |
| Mgi Id | MGI:5508934 | Doi | 10.1128/IAI.00887-13 |
| Citation | Guo Y, et al. (2013) CD30 Is Required for Activation of a Unique Subset of Interleukin-17A-Producing gammadelta T Cells in Innate Immunity against Mycobacterium bovis Bacillus Calmette-Guerin Infection. Infect Immun 81(10):3923-34 |
| abstractText | Interleukin-17A (IL-17A)-producing gammadelta T cells are known to be activated following Mycobacterium bovis bacillus Calmette-Guerin (BCG) infection. Here, we show that CD30, a member of the tumor necrosis factor (TNF) receptor superfamily, is important for activation of IL-17A-producing gammadelta T cells after BCG infection. Vgamma1(-) Vgamma4(-) gammadelta T cells preferentially expressing Vgamma6/Vdelta1 genes were identified as the major source of IL-17A in the peritoneal cavity during the early stage of BCG infection. The number of IL-17A-producing Vgamma1(-) Vgamma4(-) gammadelta T cells bearing Vgamma6 increased in peritoneal exudate cells (PEC) of wild-type (WT) mice but not in those of CD30 knockout (KO) mice in response to BCG infection. Consistently, CD30 ligand (CD30L) or CD30 expression, predominantly by Vgamma1(-) Vgamma4(-) gammadelta T cells, was rapidly upregulated after BCG infection. Inhibition of CD30L/CD30 signaling by in vivo administration of a soluble CD30 and immunoglobulin fusion protein (CD30-Ig) severely impaired activation of IL-17A-producing Vgamma1(-) Vgamma4(-) gammadelta T cells in WT mice, while stimulating CD30L/CD30 signaling by in vivo administration of agonistic anti-CD30 monoclonal antibody (MAb) restored IL-17A production by Vgamma1(-) Vgamma4(-) gammadelta T cells in CD30L KO mice after BCG infection. These results suggest that CD30 signaling plays an important role in the activation of IL-17A-producing Vgamma1(-) Vgamma4(-) gammadelta T cells bearing Vgamma6 at an early stage of BCG infection. |
