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EN
Experimental autoimmune encephalomyelitis (EAE) is an animal model of the demyelinating disease multiple sclerosis. In EAE cytokines play a critical role in defining the Th1 or Th2 nature of the autoantigen directed immune response, and in propagating and regulating inflammation within the central nervous system. In this review we summarize some of the recent developments in the field of cytokine research that relate to this model of human disease, focusing principally on disease induced with the autoantigens myelin proteolipid protein and myelin oligodendrocyte protein.
EN
Inflammation entrains a focused and coordinated response from many different elements. Soluble factors such as chemokines and cytokines direct the recruitment, differentiation, and fate of leukocytes. Cells and pathogens are killed and consumed, yet where the response is effective, inflammation will melt away, leaving a healthy functioning tissue. All this commonly takes place in an environment known as the extracellular matrix (ECM). The ECM is not a passive partner in the process and recent work demonstrates the important role that proteins found in this environment play in connecting different parts of the immune response together. In this review we will focus on these connections and the proteins that make them. One emerging trend that we will highlight is the ability of endogenous molecules to interact with receptors that are better known as sensors of the molecular fingerprints of infection. We propose that this may be particularly relevant in the context of autoimmunity, since the provision of such signals may be crucial in breaking tolerance.
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