Extended Data Fig. 7: Paracrine mechanism with endogenous CCL22 induced internalization of CCR4. | Nature Genetics

Extended Data Fig. 7: Paracrine mechanism with endogenous CCL22 induced internalization of CCR4.

From: CCL22 mutations drive natural killer cell lymphoproliferative disease by deregulating microenvironmental crosstalk

Extended Data Fig. 7

a, Immunofluorescence showing (scale bar 10 μm) the difference of CCR4 internalization between CCL22-Pro79Arg and wild type in unpermeabilized and permeabilized condition. CCR4-expressing 293 T cells were transiently transfected with the vector containing CCL22 wild type or Pro79Arg. Unpermeabilized condition only detect surface CCR4, while permeabilized condition can detect both surface and internalized CCR4. Surface CCR4 expression was decreased in wild type CCL22 but not in Pro79Arg-CCL22 mutation after 48 hours incubation. b, Serum swapping assay showing change of CCR4 expression by replacing serum of CCL22 wild type and mutant (Pro79Arg, Leu45Arg) expressing Ba/F3-CCR4 cells. Decreased CCR4 internalization (increased CCR4 expression) was observed by replacing serum of mutant CCL22 from that of CCL22 wild type, and vice versa. The mean (± SD) change rate from serum non-swapped data is shown (n = 3).

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