Poster PresentationMacrophages are the major immunocytes to initiate
both innate and adaptive immune responses against
Mycobacterium tuberculosis (Mtb), a causative agent of
tuberculosis. Upon mycoabcteria infection, macrophages
could eliminate the intracellular bacteria through different
cell death pathways, including apoptosis and autophagy.
c-Myc is a transcription factor that regulates a variety
of target genes and control different cellular functions such
as proliferation and immune resposnse. Recently, our group
revealed that c-Myc has a potential role in regulating the
antimicrobial responses in macrophages.
Here we use BCG, a live attenuated strain of
Mycobacterium bovis, which is similar to Mtb in antigenic
composition, as a model to study the role of c-Myc in
regulating mycobacteria-induced autophagy. We first
investigated the role of c-Myc in BCG-induced LC3BII
levels. Knocking down c-Myc by siRNA could decrease
BCG-induced LC3BII levels. We found that BCG-induced
autophagy is dependent on JNK and p38 and independent
on PI3K or ERK pathways. And knocking down of c-Myc
could significantly inhibit phosphorylation of p38.
In conclusion, c-Myc may play a positive role in
mycobacteria-induced autophagy in human macrophages.published_or_final_versio
