Shigella Effectors at Work - EMBO

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Gal-3 localizes to the phagosomal membrane and fusing structures Bacteria Gal-3 Immune response Proliferation Non-lectin domain Ph Development CBD B Differentiation 15-30 min Cancer progression Apoptosis, Cell cycle, Splicing, Transcription, Cell adhesion Inflammation Paz I et coll. sous presse
cytokines chemokines Inhibition of autophagy (Atg4BC74A) Ogawa M & al., Science, 2005 NF-kB NF-kB cytokines chemokines Polyubiquitinylated/SUMOylated proteins (bacteria/host cell ?), and Galectin-3 Recruitment of pro-inflammatory signaling platform (TRAF6-Ub, NEMO, NOD) Recruitment of Autophagy, sequestosome proteins (LC3, P62) Host cell membranes that compose the bacterial-containing vacuole contribute (upon rupture) as « signaling platforms » to elicit cellular innate responses. Targeting to autophagy regulates inflammation by removing degraded membranes . Paz et al., Cell.Microbiol., 2010 Ray et al., Cell Microbiol., 2010 Dupont et al., Cell Host & Microbe, 2009 Autophagy IcsA/Atg5 IcsB Deregulation of innate immune response MEF cells 2H
Page 1 and 2: Shigella effectors at work Invasion
Page 3 and 4: HISTOPATHOLOGY OF SHIGELLOSIS ELEME
Page 5 and 6: The Shigella invasion pathogenicity
Page 7 and 8: Posters of the III rd type: Marlise
Page 9 and 10: A. Zipper mechanism Invasin Yersini
Page 11 and 12: Alto et al. Ohya et al. IpgB ELMO/D
Page 13 and 14: IpaC last 72 aa fused to iota Ia co
Page 15 and 16: Rupture, invasion and inflammatory
Page 17 and 18: Adaptation of Shigella to the gut e
Page 19: GlcNAc O O CH O HCCH 3 CO CO CH 3 L
Page 23 and 24: 37°C Contact virF virB ipaC ipaB i

Shigella Effectors at Work - EMBO

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