A short treatment of the NOD mouse model of type-1 diabetes with I-BET151, a small molecule bromodomain blocker, provides long-term protection from disease by inducing macrophages to adapt an anti-inflammatory tenor whilst promoting islet β cell regeneration.
Lymphocyte migration and autoimmunity induction rely on Formin-like 1-mediated actin network remodeling to push the lymphocyte nucleus through restrictive endothelial barriers.
Potential for specific microbiome-directed, MHC-restricted shaping of a commonly selected HIV-specific CD8+ T cell population was suggested by MHC class I yeast display-based peptide screening approaches.
Targeting the differentiation regulators and/or AMPs of keratinocytes, rather than targeting immune cells, may be an alternative approach for topical anti-psoriatic treatment, an area with high need for new drugs.