Type 3 secretion effectors - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 460

(B)

(A)

(C)

FIGURE 15.2 T3SS effectors from EPEC, EHEC, and Shigella interfere with host inflammatory pathways. (A) Infection of EPEC and EHEC results in the stimu-
lation of TLRs and subsequent activation of inflammatory pathways. NleE, NleB, NleH, NleC and NleD T3SS effectors systematically dampen NF-kB and MAPK
activation by targeting key regulatory proteins such as TAB2/3, IκBα, JNK, p38, and p65. (B) Shigella activates inflammatory pathways by stimulation of both NLRs
and TLRs. OspZ, OspG, OspI, IpaH9.8, and OspF are involved in the subversion of NF-kB and MAPK pathways by targeting for example UBC13 UbcH5, NEMO/
ABIN-1, and histone H3. (C) Shigella escape autophagy by secreting IscB T3SS effector: Depending on the availability of IcsA, which is recognized by both IscB or
Atg5, Shigella can be either trapped in septin cages or spread cell-to-cell via actin-based motility.