This correspondence concerns a recent publication in Immunity by Hickman et al.1 who analyzed the effect of Cxcr3 knockout on migration of CD8+ T cells towards and within vaccinia virus-infected mouse ears. They found that Cxcr3 knockout had no effect on CD8+ T cell migration into the infected ears, a relatively mild effect on virus clearance, and an effect on the contact of CD8+ T cells with virus-infected cells. Curiously, despite having these basically sound and interesting data, Hickman et al. exaggerated the effect on virus clearance (“dramatically impaired virus clearance”) and focused their conclusions on assumed differences in migration towards infected cells (“CXCR3 chemokine receptor enables local CD8+ T cell migration”) rather than on better proven differences in binding to infected cells. I believe that from the data presented by Hickman et al. on the effect of Cxcr3 knockout a migration effect independent from the binding effect cannot be concluded beyond discussion. The fact that CXCR3 is a chemokine receptor, and that most researchers consequently expect a chemokine-gradient-dependent migration effect of the Cxcr3 knockout mutation, increases the risk of misleading readers when approached through the Hickman et al. narrative. The here-initiated discussion of their article may help to avoid such a misleading.
Correction for O'Boyle et al., Chemokine receptor CXCR3 agonist prevents human T-cell migration in a humanized model of arthritic inflammation
