CLIC1 regulates dendritic cell antigen processing and presentation by modulating phagosome acidification and proteolysis.

However CLIC1 −/− mice immunised with MOG 1-125 -pulsed CLIC1 −/− BMDCs compared to CLIC1 +/+ BMDCs, in the disease development phase, displayed less severe EAE disease that fell just short of statistical significance ( Fig. 8 C; n =6/group; P =0.064, two-way repeated-measures ANOVA).

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Indeed we found that CLIC1 −/− mice injected with CLIC1 −/− BMDCs developed less EAE than those injected with CLIC1 +/+ BMDCs, but this just failed to reach significance ( Fig. 8 C; P =0.064).

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Nevertheless, in our experimental paradigm there was an almost significant reduction in EAE between CLIC1-deficient- and replete BMDC-induced disease ( Fig. 8 C), suggesting the likelihood of reduced in vivo antigen presentation by CLIC1 −/− BMDCs.

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