Electrophilic nitro-fatty acids suppress psoriasiform dermatitis: STAT3 inhibition as a contributory mechanism.

Psoriasis is a chronic inflammatory skin disease with no cure. Although the origin of psoriasis and its underlying pathophysiology remain incompletely understood, inflammation is a central mediator of disease progression. In this regard, electrophilic nitro-fatty acids (NO-FAs) exert potent anti-inflammatory effects in several in vivo murine models of inflammatory diseases, such as chronic kidney disease and cardiovascular disease.

Colonization with Candidate Oral Probiotics Attenuates Colonization and Virulence of .

A collection of 113 strains from supragingival dental plaque of caries-free individuals were recently tested for direct antagonism of the dental caries pathogen , and for their capacity for arginine catabolism via the arginine deiminase system (ADS). To advance their evaluation as potential probiotics, twelve strains of commensal oral streptococci with various antagonistic and ADS potentials were assessed in a mouse model for oral (i.e.

mTORC2 deficiency in cutaneous dendritic cells potentiates CD8 effector T cell responses and accelerates skin graft rejection.

Mechanistic target of rapamycin (mTOR) complex (mTORC)1 and mTORC2 regulate the differentiation and function of immune cells. While inhibition of mTORC1 antagonizes dendritic cell (DC) differentiation and suppresses graft rejection, the role of mTORC2 in DCs in determining host responses to transplanted tissue remains undefined. Using a mouse model in which mTORC2 was deleted specifically in CD11c DCs (TORC2 ), we show that the transplant of minor histocompatibility Ag (HY)-mismatched skin grafts from TORC2 donors into wild-type recipients results in accelerated rejection characterized by enhanced CD8 T cell responses in the graft and regional lymphoid tissue [Correction added on January 9, 2019, after first online publication: in the previous sentence, major was changed to minor].