In contrast to these findings, and despite the bi-directional relationship between uPA and CCL2/MCP-1 [39], [40], HIV-1 infection of tonsil did not modulate the levels of soluble uPA and the number of uPA+ cells in the same tonsil histocultures (Figure 3G and Figure S2B). The gene discussed is PLAU; the disease is HIV-1 infection.