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Cells respond to conditions that impair homeostasis through ex novo synthesis of stress proteins, which differ in subcellular localization and biological function and whose differential expression depends on the type of the stressing stimulus and on the involvement of the specific stress-response signaling cascade. The biological significance of such an event is the increased resistance against further perturbations of cell homeostasis, and thus, enhanced survival. We will review briefly the available evidence concerning stress response of skeletal muscle cells, including recent results indicating the involvement of endoplasmic reticulum stress response and proteins in skeletal muscle cell differentiation and in progression of muscle diseases.

In the last few years, several reports have shown that chromatin (nucleosome) represents the main autoantigen-immunogen in systemic lupus erythematosus (SLE) and that specific antibodies are an important marker of the disease. To verify the clinical sensitivity and specificity of antinucleosome autoantibodies (ANuAs), we evaluated three ELISA immunoassay methods using different autoantigen preparations: Quanta Lite Chromatin, Medizym Anti-nucleo, and Nucleosome IgG Elisa. We compared the results with those obtained using two ELISA assays for determining anti-native DNA (anti-nDNA) antibodies: Axis-Shield and EliA dsDNA. We tested sera from 321 patients: 101 with SLE and 220 controls-48 with infectious diseases; 73 with autoimmune rheumatic disease (20 with rheumatoid arthritis, 30 with systemic sclerosis, and 23 with primary Sjögren's syndrome), and 99 healthy subjects. Using the manufacturer-recommended cutoff, the sensitivity for the three kits was 69%, 78%, and 74%, and specificity was 100%, 94.6%, and 95.0%, respectively. Using the cutoff corresponding to 95% specificity, the sensitivity of the methods for the ANuA assay was 86%, 77%, and 74%-higher than obtained with the two ELISA methods for anti-nDNA (65% and 64%). This study demonstrates that (1) the commercial reagents employed in clinical laboratories for ANuA detection show good sensitivity and high specificity; (2) ANuAs are more sensitive than anti-nDNA antibodies for diagnosing SLE; and (3) different solid-phase antigen preparations and methods used to define cutoff levels may affect a test's clinical performance.

Over the past number of years numerous data have been published regarding increased atherosclerosis in patients with systemic lupus erythematosus (SLE), and it has been shown that premature or accelerated atherosclerosis is an important cause of morbidity and mortality in these patients. Besides the traditional risk factors for cardiovascular disease, the association between SLE and atherosclerosis can be attributed to additional risk factors closely related to inflammation and autoimmunity. In particular, several autoantibodies and their respective autoantigens have been identified as possible factors in the development and progression of the atherosclerotic process in SLE. The understanding of SLE-related risk factors for enhanced atherosclerosis could shed more light on disease mechanisms, leading to new therapeutic strategies for the treatment of cardiovascular diseases in SLE patients. In the present paper, the biological characteristics and possible pathogenetic role of the oxidized low-density lipoprotein (oxLDL) and anti-oxLDL, beta(2)-glycoprotein I (beta(2)GPI) and anti-beta(2)GPI, and heat-shock protein 60/65 (HSP60/65) and anti-HSP60/65 autoantibody systems are summarized.