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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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vol. 55
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issue 1
133-156
EN
Collagens are the main components of the extracellular matrix and they constitute about 30% of total body protein. Each collagen molecule consists of three polypeptide chains that intertwine in one or more places into triple helical domains, a very rare structure in other proteins. Nineteen collagen types have been described to date and those forming banded fibrils are the most abundant. In the last decade new collagenous proteins were discovered that have been classified into three distinct groups: fibril-associated collagens with interrupted triple helices (FACITs), transmembrane collagens and multiplexins. FACITs appear to connect collagen fibrils to other matrix components or cells. Transmembrane collagens have intracellular domains and they participate in cell adhesion and probably in signal transduction. Multiplexins are situated mainly in basement membranes and contain sequences, which demonstrate features of angiogenesis inhibitors reducing the growth of neoplasmatic tumours.
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