| First Author | Tian T | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 5 | Pages | 3268-72 |
| PubMed ID | 16116218 | Mgi Jnum | J:113231 |
| Mgi Id | MGI:3664830 | Doi | 10.4049/jimmunol.175.5.3268 |
| Citation | Tian T, et al. (2005) In vivo depletion of CD11c+ cells delays the CD4+ T cell response to Mycobacterium tuberculosis and exacerbates the outcome of infection. J Immunol 175(5):3268-72 |
| abstractText | Although dendritic cells (DC) are potent APC that prime T cells against many pathogens, there is no direct evidence that DC are required for immunity to Mycobacterium tuberculosis (Mtb) infection. The requirement for DC to prime the CD4+ T cell response following Mtb infection was investigated using pCD11c-diptheria toxin receptor/GFP transgenic mice, in which DC can be transiently ablated in vivo. We show a critical role for DC in initiation of the CD4+ T cell response to the mycobacterial Ag early secretory Ag of tuberculosis 6. The delay in initiating the Ag-specific T cell response led to impaired control of Mtb replication. Interestingly, DC were not required for the secondary CD4+ T cell response following Mtb infection in peptide-vaccinated mice. Thus, this study shows that DC are essential for the initiation of the adaptive T cell response to the human pathogen Mtb. |
