Immunoregulation is an emerging paradigm of γδ T cell function. The mechanisms by which γδ T cells mediate this function, however, are not clear. Studies have identified a direct role for γδ T cells in resolving the host immune response to infection, by eliminating populations of activated macrophages. The aim of this study was to identify macrophage-reactive γδ T cells and establish the requirements/outcomes of macrophage-γδ T cell interactions during the immune response to the intracellular bacterium, Listeria monocytogenes (Lm). Using a macrophage-T cell coculture system in which peritoneal macrophages from naive or Lm-infected TCRδ−/− mice were incubated with splenocytes from naive and Lm-infected αβ/γδ T cell-deficient and wild-type mice, the ability to bind macrophages was shown to be restricted to γδ T cells and the GV5S1 (Vγ1) subset of γδ T cells. Macrophage adherence resulted in a 4- to 10-fold enrichment of Vγ1+ T cells. Enrichment of Vγ1 T cells was dependent upon the activation status of macrophages, but independent of the activation status of γδ T cells. Vγ1 T cells were cytotoxic for activated macrophages with both the binding to and killing of macrophages being TCR dependent because anti-TCRγδ Abs inhibited both Vγ1 binding and killing activities. These studies establish the identity of macrophage cytotoxic γδ T cells, the conditions under which this interaction occurs, and the outcome of this interaction. These findings are concordant with the involvement of Vγ1 T cells in macrophage homeostasis during the resolution of pathogen-mediated immune responses.

γδ T cells have a direct role in resolving the host immune response to infection by eliminating populations of activated macrophages. Macrophage reactivity resides within the Vγ1/Vδ6.3 subset of γδ T cells, which have the ability to kill activated macrophages following infection with Listeria monocytogenes (Lm). However, it is not known how γδ T cell macrophage cytocidal activity is regulated, or what effector mechanisms γδ T cells use to kill activated macrophages. Using a macrophage-T cell coculture system in which peritoneal macrophages from naive or Lm-infected TCRδ−/− mice were incubated with splenocytes from wild-type and Fas ligand (FasL)-deficient mice (gld), the ability of Vγ1 T cells to bind macrophages was shown to be dependent upon Fas-FasL interactions. Combinations of anti-TCR and FasL Abs completely abolished binding to and killing of activated macrophages by Vγ1 T cells. In addition, confocal microscopy showed that Fas and the TCR colocalized on Vγ1 T cells at points of contact with macrophages. Collectively, these studies identify an accessory or coreceptor-like function for Fas-FasL that is essential for the interaction of Vγ1 T cells with activated macrophages and their elimination during the resolution stage of pathogen-induced immune responses.

The overall surface averaged heat transfer was determined for air passing through arrays of small diameter holes drilled at 90 0 through thin metal walls. The influence of the wall metal thickness, L, was investigated for a range of hole diameters, D, and pitch, X.L/D was varied from 0.43 to 8.3 using 13 different test geometries.It was found that although the influence of L/D was significant, there was only a ±20% data scatter on a correlation of the results that ignored the influence of L/D for 0.8