Autoimmunity in the Nervous Systems: Multiple Sclerosis and Beyond 2.0

Dear Colleagues,

Several cellular and molecular mechanisms—e.g., molecular mimicry, cytokine dysregulation, dendritic cell apoptosis, and defective autophagy—underlie autoimmunity, in which factors such as sex, genes, and the environment can play different roles. Since females have been reported to be affected more often by autoimmune diseases, much attention has been given to the biological analysis of the observed sex bias and its impact on immune-mediated diseases.

One of the most recognizable and studied autoimmune diseases of the central nervous system is multiple sclerosis (MS); however, several other syndromes have been recognized, depending on the target of the immunological reaction. Interestingly, sometimes, the molecular mechanisms underlying these disorders overlap due to their common pathogenic pathways. For example, conditional deletions of autophagy-related proteins seem to protect from experimental autoimmune encephalomyelitis (the animal model of MS) and experimental arthritis. Furthermore, single-nucleotide polymorphisms (SNPs) of autophagy-related genes have been reported to be associated with susceptibility to both systemic lupus erythematosus and Crohn’s disease. In our opinion, looking into these types of interactions will also help to disentangle the complex regulation of autoimmunity, as well as providing valuable support for addressing possible novel targeted therapeutic efforts.

Following the previous Special Issue, in this new edition, we aim to broaden the current picture of autoimmunity by also considering the proven impact of gut microbiota in the immunological balance of the nervous system. Once more, particular interest will be given to novel and original data reporting significant sex differences in the autoimmune pathogenic mechanisms of the most well-known neurological diseases.

Dr. Maria Liguori
Dr. Maria Rosaria Coscia
Guest Editors

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