| First Author | Taylor SF | Year | 1997 |
| Journal | J Immunol | Volume | 159 |
| Issue | 7 | Pages | 3453-9 |
| PubMed ID | 9317144 | Mgi Jnum | J:110680 |
| Mgi Id | MGI:3640876 | Doi | 10.4049/jimmunol.159.7.3453 |
| Citation | Taylor SF, et al. (1997) Influenza infection of beta 2-microglobulin-deficient (beta 2m-/-) mice reveals a loss of CD4+ T cell functions with aging. J Immunol 159(7):3453-9 |
| abstractText | Following influenza infection, aged mice have prolonged viral shedding that is presumably due to lower anti-influenza class I-restricted CD8+ CTL activity. To examine alternative viral clearance mechanisms in immunosenescense, we infected young (1.5-2.5 month) and aged (15-18 month) class I and CD8+-deficient beta 2m-/- mice with influenza A/Port Chalmers/1/73 (H3N2). We found that 40% of young beta 2m-/- mice were shedding virus from the lung on day 9 (mean titer of 0.3 log10 TCID[50]), with a maximal anti-influenza class II CTL activity of 68+/-2% on day 7. In contrast, 100% of aged beta 2m-/- mice were still shedding virus (mean titer of 3.0 log10 TCID[50]) from the lung on day 9 with a peak CTL activity of 15+/-6%. Aged beta 2m-/- mice also had significantly lower pulmonary IFN-gamma levels, serum anti-influenza neutralizing Ab, and anti-influenza mucosal IgA titers, as well as a less intense pulmonary inflammatory response on early days of infection. Th2-mediated cytokines were dysregulated. We conclude that there are multiple mechanisms responsible for the age-related delay in recovery from influenza. These include decreased anti-influenza class II-restricted CTL activity, pulmonary IFN-gamma levels, and serum neutralizing Ab. Taken together, these findings show a loss of CD4+ T cell functions with aging. |
