Similar to previously discussed effector mechanisms of CXCR5+CD8+ T cells, in HIV infection, this subset has the ability to produce MIP-1β, IFN-γ, and/or TNF-α, but not simultaneously, a feature explained at least in part by the inhibitory effect of the PD-1–PD-L1 pathway (70). Here, CCL4 is linked to HIV infectious disease.