Cellular infiltration is a classic hallmark of
inflammation. Whereas the role of T cells in many types of
inflammation is well established, the specific impact of
antigen recognition on their migration into the site and on the accumulation of other effector cells are still matters of debate. Using a model of an inflammatory effector phase driven by
T-cell receptor (TCR) transgenic T cells, we found (i) that
antigen-specific T cells play a crucial role as 'pioneer cells' that condition the tissue for enhanced recruitment of further T effector cells and other leucocytes, and (ii) that the infiltration of T cells is not dependent on
antigen specificity. We demonstrate that a small number of
antigen-specific T cells suffice to initiate a cascade of cellular immigration into the
antigen-loaded site. Although
antigen drives this process, accumulation of T cells in the first few days of
inflammation was not dependent on T-cell reactivity to the
antigen. Both transgenic and wild-type T effector cells showed enhanced immigration into the site of
antigen challenge after the initial arrival and activation of
antigen-specific pioneer cells. This suggests that bystander accumulation of non-specific effector/memory T cells is a general feature in
inflammation. Furthermore, tumour
necrosis factor (
TNF)-alpha and
interferon (IFN)-gamma were identified as mediators that contribute to conditioning of the inflammatory site for high-rate accumulation of T effector cells in this T-cell-driven model.