Anti-Inflammatory Effects of Clarstatin, a Shared-Epitope-Antagonistic Cyclic Peptide, on Experimental Autoimmune Uveitis in Mice.

Purpose: Polymorphism and mutations of human leukocyte antigens (HLAs) and calreticulin are risk factors for uveitis. Here, we sought to determine the therapeutic effects of Clarstatin, a cyclic peptide antagonist of the HLA shared-epitope-calreticulin interaction, in experimental autoimmune uveitis (EAU) models.

Methods: Mice were injected with Clarstatin intraperitoneally and its effect was compared to that of corticosteroid.

CD47 and thrombospondin-1 contribute to immune evasion by .

is a gram-negative anaerobic bacterium linked to periodontal disease. Remarkably, thrives in an inflamed environment rich in activated neutrophils. Toll-like receptor 2 (TLR2) recognition is required for to evade innate immune killing; however, the mechanisms through which uncouples host inflammation from bactericidal activity are only partially known.

-Induced TLR2 Interactome Analysis Reveals Association with PARP9.

is a Gram-negative anaerobic bacterium strongly associated with periodontal disease. Toll-like receptor 2 (TLR2) is indispensable for the host response to , but escapes from immune clearance via TLR2-dependent activation of phosphoinositide-3-kinase (PI3K). To probe the TLR2-dependent escape pathway of , we analyzed the TLR2 interactome induced following infection or activation by a synthetic lipopeptide TLR2/1 agonist on human macrophages overexpressing TLR2.

Porphyromonas gingivalis induction of TLR2 association with Vinculin enables PI3K activation and immune evasion.

Porphyromonas gingivalis is a Gram-negative anaerobic bacterium that thrives in the inflamed environment of the gingival crevice, and is strongly associated with periodontal disease. The host response to P. gingivalis requires TLR2, however P.