Multiple sclerosis (MS) develops in young adults with a complex predisposing genetic trait and probably requires an inciting environmental insult such as a viral infection to trigger the disease. The activation of CD4+ autoreactive T cells and their differentiation into a Th1 phenotype are a crucial events in the initial steps, and these cells are probably also important players in the long-term evolution of the disease. Damage of the target tissue, the central nervous system, is, however, most likely mediated by other components of the immune system, such as antibodies, complement, CD8+ T cells, and factors produced by innate immune cells. Perturbations in immunomodulatory networks that include Th2 cells, regulatory CD4+ T cells, NK cells, and others may in part be responsible for the relapsing-remitting or chronic progressive nature of the disease. However, an important paradigmatic shift in the study of MS has occurred in the past decade. It is now clear that MS is not just a disease of the immune system, but that factors contributed by the central nervous system are equally important and must be considered in the future.

Immunology of multiple sclerosis

The remarkable capacity of the mammalian immune system to coordinate deadly attacks against numerous invading pathogens, yet turn a blind eye to self-tissues continues to fascinate immunologists. It has been clear for some time that immune cells capable of recognizing self-proteins exist in normal individuals without seemingly causing harm. The 'peripheral tolerance' mechanisms that keep these cells in check are the focus of intense research, not least because defects in these pathways might cause autoimmune diseases. In this review, new developments in our understanding of peripheral tolerance are discussed.

The enemy within: keeping self-reactive T cells at bay in the periphery

Autoimmune disease is the consequence of an immune response against self-antigens that results in the damage and eventual dysfunction of target organs. Although the triggering event in most autoimmune diseases is unknown, an infectious cause has long been postulated to explain the development of autoimmunity. Molecular mimicry is one mechanism by which infectious agents (or other exogenous substances) may trigger an immune response against autoantigens. According to this hypothesis a susceptible host acquires an infection with an agent that has antigens that are immunologically similar to the host antigens but differ sufficiently to induce an immune response when presented to . . .

Molecular Mimicry and Autoimmunity

Deconstructing the Peptide-MHC Specificity of T Cell Recognition

The immunologic specificity of the antigen receptors of T cells and B cells is the result of random shuffling of the many genes that form the DNA code for the antigen-binding site of these receptors.1–3 Theoretically, this process could generate 109 different T-cell receptors, including some that can bind to autoantigens (these cells are often called self-reactive T cells). Tolerance is the process that eliminates or neutralizes such autoreactive cells, and a breakdown in the working of this system can cause autoimmunity. B-Cell Tolerance Autoantibodies are characteristic of many autoimmune diseases and may be the direct cause of the . . .

Tolerance and Autoimmunity

Predictable TCR antigen recognition based on peptide scans leads to the identification of agonist ligands with no sequence homology

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Predictable TCR antigen recognition based on peptide scans leads to the identification of agonist ligands with no sequence homology