The activation of T cell in secondary lymphoid organs in a well-studied phenomenon. How these activated T cells go on to reencounter cognate antigen presenting cells at sites of infection and inflammation is less well understood, however. T cell activation at these locations, such as in tumors, is critical for controlling and clearing disease. CXCR3-CXCL10 signaling has been shown to position T cells for crucial stimulatory cues in the lymph node and we show here that this signaling axis remains critical in inflamed, non-lymphoid tissues. Following the introduction of type-1 pro-inflammatory stimuli to skin via L.major infection or CFA/OVA immunization immune cells, primarily monocytes and neutrophils, are recruited to and cluster within the inflamed tissue. Monocytes then begin to upregulate CXC10 and MHCII expression to facilitate T cell recruitment to and activation within the local tissue space. We showed that in the absence of monocytes T cells are unable to produce IFN. This initial T cell activation is integral to mounting a potent immune response as their resulting IFN production drives further CXCL10 expression and cell recruitment to ramp up local inflammation. Strikingly, we found that in the absence of CD4 T cells, CXCL10+ monocyte clusters failed to form despite their maintained recruitment to the skin. This indicated to us that T cells play a crucial role in organizing their own activation niches. Further studies revealed that CXCR2 signaling was required for this T cell mediated clustering of monocytes in the skin. Together these studies highlight the importance of monocytes as antigen presenting cells, and a novel role for CD4 T cells to organize myeloid subsets to better facilitate further T cell activation.