Integrins, expressed on virtually every cell type, are proteins that mediated cellular interactions with components of the extracellular matrix (ECM) and cell surface integral plasma membrane proteins. In addition, integrins interact with the cytoskeleton and through this process participate in cell migration, tissue organization, cell growth, haemostasis, inflammation, target recognition of lymphocytes and the differentiation of many cell types. Signals generated from ligand-integrin interactions are propagated via the integrin cytoplasmic tails to signal transduction pathways within the cell (outside-in signalling). Information from within the cell can also be transmitted to the outside via integrin affinity modulation (inside-out signalling). Protein tyrosine phosphorylation has a central role in integrin-initiated cell signalling, leading to cytoskeletal organization and focal adhesion formation. This review will examine the current understanding of integrin function, focusing on the intracellular consequences of integrin-ligand interaction.
Although the etiology of systemic lupus erythematosus (SLE) remains enigmatic, it is likely that antibodies to DNA are an integral component in many, though not all, cases. The caveat is necessary, because several reports (for review, see ref. 1) have indicated that 30% or more of patients who meet the widely accepted classification criteria (2) devised by the American College of Rheumatology (formerly, the American Rheumatism Association) do not have detectable anti-DNA antibodies. Although useful, the classification criteria are broadly based and allow the diagnosis of SLE in patients with diverse clinical and serologic features. Most patients without anti-DNA antibodies do have antinuclear antibodies of other specificities (e.g., anti-Sm, anti-Ro, anti-La). It is possible, though we doubt it, that more sensitive assays would detect anti-DNA antibodies in all SLE patients. Thus on balance, lupus should really be considered a generic term, encompassing several individual conditions.The presence of anti-DNA antibodies in the serum of SLE patients has long been considered both a marker of, and pathologic factor in, renal disease (3,4). Indeed, in our group of nearly 200 SLE patients, we have yet to see a patient with severe renal involve-
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