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Cytomegaloviruses (CMV) can cause disease in immunocompromised individuals. Natural Killer (NK) cells are a natural defense against viral infection as they scan cells for activating or inhibitory markers. CD155 (PVR) can trigger different reactions depending on the ligand the target cell expresses.
  • DNAM-1 (CD226) leads to activation.
  • TIGIT inhibits immune responses.
  • CD96 can both activate and inhibit the cell.
Rovis et al. wanted to investigate how CMV can manipulate immune responses. They found that the m20.1 viral protein decreased expression of PVR. NK cells can express DNAM-1 and TIGIT, the latter of which has a higher affinity for PVR. As such, the lower expression of PVR on the virally-infected cell increases the likelihood that the NK cell will be shut down by TIGIT ligation. On the other hand, inflammatory monocytes only express DNAM-1 and can still be drawn in by CCL2. Their activation leads to IL-12 production, which activates DNAM-1+ NK cells to release IFN-γ. This system demonstrates how the body can still defend against CMV infection even if NK cells are inhibited by PVR-TIGIT interactions. BioLegend provides several new conjugated antibodies for PVR and DNAM-1 analysis in flow cytometry.
Adapted from Rovis, et al. 2016. J. Exp. Med. 213:1835. Pubmed
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Specificity Human Mouse
CD96 NK92.39 3.3
CD155 SKII.4, TX24 4.24.1, TX56
CD226 (DNAM-1) 11A8, TX25 10E5, 480.1, TX42.1
TIGIT A15153G 1G9
CCL2 2H5, 5D3-F7 2H5
IFN-γ 4S.B3, B27 XMG1.2
IL-12 C11.5 C15.6
Human Mouse
CCL2 CCL2
IFN-γ IFN-γ
IL-12/IL-23 (p40) Mouse IL-12/IL-23 (p40)
IL-12p70 Mouse IL-12p70
Human Mouse
CCL2 CCL2
IFN-γ IFN-γ
IL-12p70 Mouse IL-12 (p40)
  Mouse IL-12p70
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