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The central role of co-stimulatory and co-inhibitory receptors in T cell biology has been proven by the effective therapeutic targeting of some of these molecules. However, the molecular aspects of T cell co-stimulation and co-inhibition are far from being fully understood. Here, the authors discuss emerging concepts in T cell co-signalling.
Type 1 diabetes (T1D) was described as an autoimmune disease more than 25 years ago, but the mechanisms involved in this disease are not yet completely understood. Here, the authors review the current models of how T1D disease develops and discuss the steps that will need to be taken to develop more successful therapies for patients.
The first signalling molecules that are activated following T cell receptor engagement feed into an intricately branched and tightly regulated network of signalling cascades that influences T cell activation and differentiation. Perturbation of this diversified network can result in dysregulated T cell signalling and the development of autoreactivity.
The lymphotoxin signalling pathway is best known to immunologists for its crucial roles in promoting the development and the organization of lymphoid organs. However, lymphotoxin also contributes to protective immunity against infection and can regulate the intestinal microbiota. The authors discuss these and the other lesser known immune functions of lymphotoxin.
Population genetics informs about how genes have evolved under varying selective pressures. The analysis of such selection signatures in innate immune genes, including genes encoding pattern-recognition receptors and their downstream effector molecules, provides helpful insight into the roles of these genes in host immunity and their links to disease.
If an exogenous antigen such as gluten can drive the autoimmune features of coeliac disease, such as the production of autoantibodies and the destruction of a specific tissue type, should we be looking more closely at the possibility that other autoimmune diseases are driven by exogenous, not self, antigens?