| First Author | Khanolkar A | Year | 2004 |
| Journal | J Immunol | Volume | 172 |
| Issue | 5 | Pages | 2834-44 |
| PubMed ID | 14978084 | Mgi Jnum | J:88234 |
| Mgi Id | MGI:3029803 | Doi | 10.4049/jimmunol.172.5.2834 |
| Citation | Khanolkar A, et al. (2004) CD4 T cell-dependent CD8 T cell maturation. J Immunol 172(5):2834-44 |
| abstractText | We have investigated the contribution of CD4 T cells to the optimal priming of functionally robust memory CD8 T cell subsets. Intranasal infection of CD4 T cell-deficient (CD4(-/-)) mice with lymphocytic choriomeningitis virus resulted in the elaboration of virus-specific CD8 T cell responses that cleared the infection. However, by comparison with normal mice, the virus-specific CD8 T cells in CD4(-/-) mice were quantitatively and qualitatively different. In normal mice, lymphocytic choriomeningitis virus-specific memory CD8 T cells are CD44(high), many are CD122(high), and a majority of these cells regain expression of CD62L overtime. These cells produce IFN-gamma and TNF-alpha, and a subset also produces IL-2. In the absence of CD4 T cell help, a distinct subset of memory CD8 T cells develops that remains CD62L(low) up to 1 year after infection and exhibits a CD44(int)CD122(low) phenotype. These cells are qualitatively different from their counterparts in normal hosts, as their capacity to produce TNF-alpha and IL-2 is diminished. In addition, although CD4-independent CD8 T cells can contain the infection following secondary viral challenge, their ability to expand is impaired. These findings suggest that CD4 T cell responses not only contribute to the optimal priming of CD8 T cells in chronically infected hosts, but are also critical for the phenotypic and functional maturation of CD8 T cell responses to Ags that are more rapidly cleared. Moreover, these data imply that the development of CD62L(high) central memory CD8 T cells is arrested in the absence of CD4 T cell help. |
