| First Author | Smith P | Year | 2001 |
| Journal | Eur J Immunol | Volume | 31 |
| Issue | 5 | Pages | 1495-502 |
| PubMed ID | 11465106 | Mgi Jnum | J:69510 |
| Mgi Id | MGI:1934749 | Doi | 10.1002/1521-4141(200105)31:5<1495::AID-IMMU1495>3.0.CO;2-8 |
| Citation | Smith P, et al. (2001) Defective in vivo induction of functional type 2 cytokine responses in aged mice. Eur J Immunol 31(5):1495-502 |
| abstractText | Aged mice have various defects in their immune system. We report that following in vivo challenge with type 2 cytokine-inducing Schistosoma mansoni eggs, aged mice fail to produce type 2 cytokines and also have impaired antigen-specific antibody production. Using two separate type 2 cytokine-dependent in vivo models, the synchronous pulmonary schistosome egg granuloma model and infection with the gastro-intestinal nematode Nippostrongylus brasiliensis, aged mice were shown to have a dramatically impaired capacity to elicit a functional type 2 response, i. e. respectively, impaired pulmonary granulomas and delayed rejection of intestinal worms. Aged mice did not develop eosinophilia and had impaired production of antigen specific IgE. Defective induction of type 2 responses was associated with negligible IL-2 and elevated IFN-gamma production by cells from aged mice. Naive aged mice had increased numbers of Th1, Th2 and Tc1 cells compared to young animals. In vivo type 2 challenge increased the frequencies of Th1 and Tc1 cells and reducing Th2 cell numbers in aged mice. These data demonstrate that a consequence of ageing is a profound in vivo defect in the capacity to elicit type 2 cytokine responses and such an impairment in type 2 responsiveness may account for the increased incidence of various type 1 cytokine-mediated diseases in aged individuals. |
