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Innate immune recognition of breast tumor cells mediates CCL22 secretion favoring Treg recruitment within tumor environment

, , , , &
Pages 759-761 | Published online: 24 Aug 2012

Figures & data

Figure 1. Scheme recapitulating the sequence of events leading to the strong non polarized CCL22 production by tumor cells. Healthy epithelial cells secrete low levels of CCL22 in a polarized manner within the luminal acini, their transformation favor their recognition by infiltrating NK cells leading to IFNγ secretion. IFNγ promoted macrophage activation that will produce TNFα and IL-1β after interaction with breast epithelial tumor cells. Combined action of IFNγ, IL-1β and TNFα will induce non polarized strong CCL22 secretion by tumor cells that will induce the recruitment of CCR4+ Treg from periphery, leading to CCR4 internalization.

Figure 1. Scheme recapitulating the sequence of events leading to the strong non polarized CCL22 production by tumor cells. Healthy epithelial cells secrete low levels of CCL22 in a polarized manner within the luminal acini, their transformation favor their recognition by infiltrating NK cells leading to IFNγ secretion. IFNγ promoted macrophage activation that will produce TNFα and IL-1β after interaction with breast epithelial tumor cells. Combined action of IFNγ, IL-1β and TNFα will induce non polarized strong CCL22 secretion by tumor cells that will induce the recruitment of CCR4+ Treg from periphery, leading to CCR4 internalization.