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Integrin alpha-1 beta-1 (α1β1), also known as Very Late Antigen-1 (VLA-1), is a heterodimeric transmembrane receptor composed of the α1 (CD49a) and β1 (CD29) subunits [4, 9, 10]. It serves as a major cell surface receptor for collagen types I and IV and laminin, playing a critical role in cell-matrix adhesion and bidirectional signal transduction [9, 18]. α1β1 is expressed on various cell types, including smooth muscle cells, fibroblasts, and activated leukocytes, and is recognized as a definitive marker for tissue-resident memory T cells (Trm) [9, 17]. In disease states, it is a significant mediator of chronic inflammation, such as rheumatoid arthritis and inflammatory bowel disease, by facilitating the recruitment and retention of inflammatory cells in tissues [1, 3, 5]. It is also implicated in the regulation of angiogenesis, fibrosis, and cancer progression [3, 4, 17]. Therapeutic strategies targeting α1β1, such as the monoclonal antibody SAN-300, aim to block its interaction with the extracellular matrix to reduce inflammatory responses and tissue remodeling [1, 2, 5].
Inhibition of the interaction between the integrin alpha-1 beta-1 heterodimer and its extracellular matrix ligands, such as collagen and laminin, thereby modulating cell adhesion, migration, and inflammatory signaling.
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