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mechanisms of interaction with flagellin and profilin
Data show that TLR11 expression is induced in astrocytes, neurons, and microglia in the immune response to T. gondii infection
TLR11 mediates innate immune function of male germ cells in response to T. gondii profilin and uropathogenic escherichia coli stimulations.
Biochemical experiments revealed that TLR11 and TLR12 directly bind to Toxoplasma gondii profilin and are capable of forming a heterodimer complex.
Selective elimination of neutrophils in TLR11-deficient mice infected with Toxoplasma gondii results in acute susceptibility similar to that observed in IFN-gamma-deficient mice.
While parasite RNA and DNA activate innate immune responses via TLR7 and TLR9, TLR11 and TLR12 heterodimers are required for sensing and responding to Toxoplasma profilin infection.
a potentially important role for TLR11 in preventing murine intestinal infection and modulating antigen transportation in the gut and imply an important role for various TLRs in cooperation with tight control of pathogens penetrating into Peyer patches.
association with UNC93B1 and the intracellular localization of TLRs are not unique features of nucleic acid-sensing TLRs but is also essential for TLR11-dependent recognition of T. gondii profilin and for host protection against this parasite
Data demonstrate that transcription of the Tlr11 gene is regulated through epithelium-specific transcription factors and IRF-8.
displays a distinct pattern of expression in macrophages and liver, kidney, and bladder epithelial cells; mice lacking TLR11 are highly susceptible to infection of the kidneys by uropathogenic bacteria
Toxoplasma gondii profilin activates dendritic cells through TLR11 and is the first chemically defined ligand for this TLR; TLR11 is required in vivo for parasite-induced IL-12 production and optimal resistance to infection
The immunogenicity of Toxoplasma gondii profilin was entirely dependent on both TLR11 recognition and signaling through the adaptor myeloid differentiation factor 88 (MyD88).
TLR11-deficient mice develop an abnormal immunopathological response to Toxoplasma gondii, as the result of non-toll-like receptor dependent activation of interferon-gamma secretion by natural killer cells in response to the infection.
TLRs 11-13 are expressed in normal and parasite infected mouse brains. This suggests a role for them in central nervous system infections.
Participates in the innate immune response to microbial agents. Acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response (By similarity).