Voie d'immunisation et séquence d'administration de l ... - TEL

tel-00827710, version 1 - 29 May 2013
and received poly I:C 7 hours post-immunization. This time point was known from previous
work to induce an inhibition of priming (Figure 39). On day 3 post-immunization, CFSE-
labeled antigen-specific OT-I T cells were transferred into the mice and 3 days later, OT-I
division was assessed by looking at CFSE dilution. If DCs presenting antigen were present,
OT-I would proliferate. As shown in Figure 41A, OT-I transferred into WT recipients did not
divide in the non-immunized animals whereas a robust proliferation can be observed in
immunized mice. As expected, inhibition of OT-I division in immunized mice was conferred
by poly I:C treatment 7 hours post-immunization. In contrast, the same level of OT-I
proliferation was observed in IFNAR -/- recipients that had been immunized, irregardless of
their treatment with poly I:C (Figure 41B). These results demonstrated that in WT recipients
there are not DCs available to cross-present antigen after poly I:C injection and this
phenomena is type I IFN-dependent.
Figure 41. Inhibition of cross-presentation by poly I:C is type I IFN-dependent. WT and IFNAR -/-
mice were immunized i.d. with 5x10 5 K bm1 mOva splenocytes and received 100µg of poly I:C 7 hours
later. On day 3, 5x10 6 CD45.1 + CFSE-labeled OT-I were transferred and CFSE dilution was evaluated
3 days later. Representative results of CFSE dilution of CD8 + OT-I cells obtained from WT mice are
shown (A). The percentage of undivided OT-I was determined and plotted (B) for WT and IFNAR -/-
mice. p-values were calculated using a Mann-Whitney test. NI, non-immunized mice.
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