Modulation of nuclear factor-kappaB activity can influence the susceptibility to systemic lupus erythematosus.

Autoimmune diseases, such as systemic lupus erythematosus (SLE), result from deficiencies in self-antigen tolerance processes, which require regulated dendritic cell (DC) function. In this study we evaluated the phenotype of DCs during the onset of SLE in a mouse model, in which deletion of the inhibitory receptor FcgammaRIIb leads to the production of anti-nuclear antibodies and glomerulonephritis. Splenic DCs from FcgammaRIIb-deficient mice suffering from SLE showed increased expression of co-stimulatory molecules.

Activating and inhibitory Fcgamma receptors can differentially modulate T cell-mediated autoimmunity.

The molecular bases responsible for the loss of T cell tolerance to myelin antigens leading to the onset of multiple sclerosis remain obscure. It has been shown that balanced signaling through activating and inhibitory receptors is critical for the maintenance of tolerance to self antigens in autoimmune disorders. However, although FcgammaR have been shown to influence experimental autoimmune encephalomyelitis (EAE) development, their role during pathogenesis remains controversial.

Inhibition of nuclear factor-kappa B enhances the capacity of immature dendritic cells to induce antigen-specific tolerance in experimental autoimmune encephalomyelitis.

Autoimmune disorders develop as a result of deregulated immune responses that target self-antigens and cause destruction of healthy host tissues. Because dendritic cells (DCs) play an important role in the maintenance of peripheral immune tolerance, we are interested in identifying means of enhancing their therapeutic potential in autoimmune diseases. It is thought that during steady state, DCs are able to anergize potentially harmful T cells bearing T cell receptors that recognize self-peptide-major histocompatibility complexes.

The dendritic cell-T cell synapse as a determinant of autoimmune pathogenesis.

Autoimmune diseases occur when the immune response is targeted to self-antigens, leading to destruction or altered function of specific cells and tissues. Although the aetiology of these diseases has not yet been fully elucidated, it is believed that genetically determined susceptibility and environmental triggers are both implicated in the detrimental immune response against the body's own tissues. Dendritic cells (DCs) are professional antigen presenting cells that play an important role in maintaining peripheral tolerance by preventing self-reactive T cells from causing autoimmune damage.

Molecular interactions between dendritic cells and Salmonella: escape from adaptive immunity and implications on pathogenesis.

Dendritic cells (DCs) constitute the link between innate and adaptive immunity by directly recognizing pathogen-associated molecular patterns (PAMPs) on bacteria and by processing and presenting bacterial antigens to T cells. Recognition of PAMPs renders DCs as professional antigen-presenting cells with the ability to prime naive T cells and to initiate the adaptive immune response against pathogen-derived antigens. For this reason, any interference with DC function might be advantageous for bacterial survival and dissemination.

Andrographolide interferes with T cell activation and reduces experimental autoimmune encephalomyelitis in the mouse.

Andrographolide is a bicyclic diterpenoid lactone derived from extracts of Andrographis paniculata, a plant indigenous to South Asian countries that shows anti-inflammatory properties. The molecular and cellular bases for this immunomodulatory capacity remain unknown. Here, we show that andrographolide is able to down-modulate both humoral and cellular adaptive immune responses.