| T cells are a critical aspect of the immune system. In humans, their absence results in a high susceptibility to infection and eventual death. Integrins are involved in many aspects of T cell life, including naive T cell circulation, activation, and effector/memory T cell localization. In this work, we evaluate the particular role of beta1 integrin in CD4 T cell function. In order to do this in a mammalian system, we developed mice specifically lacking beta1 integrin on T cells. We demonstrate that these mice have normal numbers and localization of naive T cells. Yet, we find beta1-deficient T cells have enhanced alpha4beta7 integrin expression leading to an increased number of memory T cells in the gut. This work reveals a novel mechanism for the regulation of alpha4beta7 expression driven by the preferential pairing of beta1 integrin with alpha4 integrin on CD4 T cells. Memory CD4 T cells lacking beta1 integrin also have decreased maintenance in the bone marrow, which is proposed to be a critical 'survival niche' for T cell memory. Surprisingly, we demonstrate that the maintenance of memory CD4 T cells in the bone marrow by beta1 integrin is not required for long-term CD4 T cell memory. Overall, this work has implications for the intentional modulation of integrin expression and the control of T cell localization in the body. |
