| First Author | Flynn S | Year | 2003 |
| Journal | Blood | Volume | 101 |
| Issue | 11 | Pages | 4472-8 |
| PubMed ID | 12543861 | Mgi Jnum | J:151744 |
| Mgi Id | MGI:4355133 | Doi | 10.1182/blood-2002-10-3030 |
| Citation | Flynn S, et al. (2003) Tumor and CD4 T-cell interactions: tumor escape as result of reciprocal inactivation. Blood 101(11):4472-8 |
| abstractText | This paper addresses the capacity of naive, effector, and memory CD4 T cells to control growth of a major histocompatibility complex (MHC) class II-positive B-cell lymphoma in vivo. To assess the role of T cells on their own without contributions by B cells, antibodies, or natural killer (NK) cells, we generated pure effector or memory CD4 T cells in Rag-/-gc-/- mice deficient in endogenous lymphocytes and NK cells. Lymphoma cells expressing a model antigen were injected into mice with T cells of cognate specificity that were either naive or in effector or resting memory state. Naive T cells were unable to prevent tumor growth, probably due to delay of efficient cross-presentation by dendritic cells. However, both effector and memory T cells, dependent on the amount of antigen available, controlled the tumor for a considerable period of time without the need for dendritic cell stimulation. Nevertheless, the tumor eventually grew uncontrolled in all cases. This was not because of a defect in T-cell homing to the tumor site or loss of MHC class II or costimulatory molecules by the tumor, but reflected mutual paralysis of T-cell responsiveness and antigen processing by tumor cells. |
