Abstract
Histamine is a biogenic amine with a broad spectrum of activities in various physiological and pathological situations. Besides its well-characterised effects in allergic responses and in acute inflammation, histamine modulates the cytokine network, influencing T helper 1 and T helper 2 balance, and antibody isotype. In multiple sclerosis (MS), and its animal model of experimental autoimmune encephalomyelitis (EAE), there are several steps in the autoimmune attack against myelin of the central nervous system where histamine might play an important role. Indeed, blockade of specific histamine receptors has been proven to prevent early acute EAE by reducing encephalitogenic T helper 1 response and altering antigen presentation. A deeper understanding of the mechanisms by which histamine regulates the development and progression of EAE and MS might open new strategies for immune intervention.
Keywords: dendritic cells, histamine receptor, G-protein-coupled receptors, vasoactive amine sensitisation (VAAS), experimental autoimmune encephalomyelitis