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The interaction between the extracellular matrix (ECM) and the immune system is a fundamental regulatory axis that maintains tissue homeostasis and coordinates responses to injury. The ECM is not merely a passive scaffold but a dynamic reservoir of biochemical signals that influence immune cell recruitment, differentiation, and activation through receptors such as integrins and CD44 (Source: Sorokin, L., Nature Reviews Immunology, 2010). Conversely, immune cells actively remodel the ECM by secreting proteases like matrix metalloproteinases (MMPs), which can release sequestered growth factors or generate bioactive fragments known as matrikines that further modulate immune signaling (Source: Journal of Cell Science, 2020). Dysregulation of this bidirectional crosstalk is a hallmark of various pathologies, including chronic inflammatory diseases and fibrosis. In the context of oncology, an altered or stiffened ECM can create a physical barrier that excludes cytotoxic T cells while promoting an immunosuppressive microenvironment that facilitates tumor progression (Source: EMBO Reports, 2014). While specific components within this axis, such as integrin alpha-V beta-3 or hyaluronidase, are investigated as therapeutic targets, the 'Extracellular matrix and immune system' as a whole describes a complex biological context rather than a single druggable molecule.
Not applicable as this represents a biological system or interaction network rather than a single molecular target.
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