In some cases, a transient autoimmune process can occur as a result of an infection. This may be due to molecular mimicry between the pathogen and a self-antigen, or to the release of normally sequestered self-antigens due to tissue damage from the infection. An important factor leading to these autoreactive immune responses is the activation of dendritic cells by the infection-induced inflammation. Once the infection is resolved, this inflammation will also subside. As a consequence, autoreactive T cells may no longer receive sufficient signals to promote their activation, causing a remission in the autoimmune symptoms. One important change in antigen-presenting dendritic cells during an infection that would contribute to the activation of normally self-tolerant self-reactive T cells is:
A) The down-regulation of phagocytic activity by activated dendritic cells
B) The up-regulation of MHC class I and class II molecules on activated dendritic cells
C) The increased production of Type I interferons by activated dendritic cells
D) The increased expression of cytoplasmic nucleic acid sensors by activated dendritic cells
E) The down-regulation of anti-inflammatory cytokines, such as IL-10, by activated dendritic cells
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