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. Author manuscript; available in PMC: 2011 Mar 1.
Published in final edited form as: Immunol Rev. 2010 Mar;234(1):163–176. doi: 10.1111/j.0105-2896.2009.00867.x

Fig. 2. Effects of the interaction between BST2 and ILT7 on pDCs.

Fig. 2

(Top) By sensing viral infection, pDCs can rapidly and rigorously produce large amounts of type I IFN via TLR7 or TLR9 activation. IFN then may induce the neighboring cells to express BST2, which in turn engages with ILT7 on pDCs to downregulate the magnitude of IFN and cytokine responses in a negative-feedback manner. (Bottom left) In a tumor environment where BST2 is endogenously expressed, infiltrating pDCs may be functionally suppressed to elicit normal IFN response to TLR ligands as a result of the interaction between BST2 and ILT7. (Bottom right) When coexpressed, ILT7 sequesters BST2 by inducing BST2 internalization as a result of cis-recognition.