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Autologous Stem Cell Transplantation in Relapsing Polychondritis
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Falk Hiepe, Andreas Thiel, Oliver Rosen, Gero Massenkeil, Gerd-Rüdiger Burmester, Andreas Radbruch, Renate Arnold
Although relapsing polychondritis is a separate clinical entity, up to 30% of patients also suffer from another inflammatory disease (Table 1). The most common associated disease is vasculitis, which can affect vessels of all sizes. Five to 14% of all patients with relapsing polychondritis have biopsy-confirmed leukocytoclastic vasculitis, ranging from isolated cutaneous leukocytoclastic vasculitis to aortitis. Although vasculitis most commonly leads to dilatation of the aortic ring and ascending aorta, aneurysm of the descending thoracic or abdominal aorta can also occur. Aortic rupture has also been reported. Dermatological and renal manifestations, neuropathies, audiovestibular abnormalities, and episcleritis are most likely due to microscopic angiitis. Vasculitis seems to worsen the prognosis of relapsing polychondritis.17 Relapsing polychondritis is infrequently accompanied by defined vasculitides like Wegener’s granulomatosis and polyarteritis nodosa.18 The co-occurrence of relapsing polychondritis and Behcet’s disease has also been reported; this constellation was named “MAGIC syndrome” (mouth and genital ulcers with inflamed cartilage syndrome).19 Roughly 25% of patients with relapsing polychondritis have associated autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, mixed connective tissue disease, Sjogren’s syndrome, and hypothyroidism.
Immunofluorescence
Published in Guy Cox, Fundamentals of Fluorescence Imaging, 2019
IIF testing led to the detection of autoantibodies in various autoimmune diseases, including systemic lupus erythematosus, scleroderma, dermatomyositis, and mixed connective tissue disease. Certain autoantibodies produced distinct patterns of staining since they reacted with specific organelles in the nucleoplasm, nuclear membrane, nucleolus, or cytoplasm. An outstanding example is an autoantibody in the CREST (calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) subset of scleroderma, in which immunostaining revealed a limited number of dots in the nucleoplasm of interphase cells, but a total redistribution of these dots to the centromeric regions of condensed chromosomes of cells in mitosis. It became clear that there were multiple autoantibodies of different specificities in any individual autoimmune disease, a few autoantibodies were disease specific, and different autoantibody profiles were associated with different diseases [48].
Nanotubes and Nanowires for Biosensing
Published in George K. Knopf, Amarjeet S. Bassi, Smart Biosensor Technology, 2018
Since the nonspecific adsorption of biomolecules on the CNTFET surface is not always desirable, such binding should be avoided to improve the selectivity and specificity of the biosensing system. Polymer coating layers including PEI, PEG, polyethyleneoxide, and Tween on CNTs have been used to capture biomolecules with a high degree of control and specificity, whereas low-affinity species will be rejected [78,88]. The amino groups in irreversibly tethered polymer molecules on CNTs permit coupling of biotin or antigen probes, which still retain their antigenicity for binding their respective streptavidin or antibody with high specificity. For example, the binding of 10E3 mAbs antibody, a prototype target of the autoimmune response in patients with systemic lupus erythematosus and mixed connective tissue disease, to a recombinant human autoantigen U1A protein (a 33-kDa protein, extracted from insect cells) has been monitored in real time electronically using a CNTFET-based sensing system [68] (Figure 4.19). For this proposal, U1A protein was immobilized on Tween-coated CNTs to capture the respective 10E3 mAbs antibody. The detection limit is lower than 1 nM, which favorably compares with the detection limit (2.3 nM) based on fluorescence array analysis.
Mine-site derived particulate matter exposure exacerbates neurological and pulmonary inflammatory outcomes in an autoimmune mouse model
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Alexis Wilson, Carmen A. Velasco, Guy W. Herbert, Selita N. Lucas, Bethany N. Sanchez, José M. Cerrato, Michael Spilde, Quan-Zhen Li, Matthew J. Campen, Katherine E. Zychowski
Serum neutrophil elastase was assessed via ELISAs (enzyme-linked immunoassay) from a commercial vendor (Signosis, Santa Clara, CA). Using a proteomic microarray containing autoantigens (UT Southwestern), serum IgG and IgM autoantibodies were also determined in a high-throughput platform from exposed and unexposed treatment groups. Key autoantigens included in the panel were selected based upon recent relevant autoimmune literature including, but not limited to Sjøgren’s syndrome, scleroderma, polymyositis, systemic lupus erythematosus, mixed connective tissue disease, polymyositis and rheumatoid arthritis. Selected autoantigens were adjusted to final concentration of 1 mg/ml with PBS and immobilized onto nitrocellulose membrane-coated glass slides using a non-contact micro-dispenser Nonoplotter NP2.1 (GeSim, Gemany). A 1:50 dilution of mouse serum was incubated with the array and anti-mouse IgG and anti-mouse IgM secondary antibodies tagged with two differing fluorophores (cy3 for IgG and cy5 for IgM) were used to determine autoantibody levels in each sample (Rajasinghe et al. 2020).
Autoantibodies and cancer among asbestos-exposed cohorts in Western Australia
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Renee N Carey, Jean C Pfau, Marvin J Fritzler, Jenette Creaney, Nicholas de Klerk, Arthur W (Bill) Musk, Peter Franklin, Nita Sodhi-Berry, Fraser Brims, Alison Reid
In this study, the relationship between ANA and asbestos-associated cancers was examined, since amphibole asbestos exposures were shown to induce ANA (Pfau et al. 2005), and because of some evidence that autoimmune responsiveness is associated with, and may play roles in, development of some cancers (Chapman et al. 2008; Macdonald, Parsy-Kowalska, and Chapman 2017; Noble et al. 2016). Anti-nuclear autoantibodies are strongly associated with, and sometimes diagnostic for, systemic autoimmune diseases including systemic lupus erythematosus (SLE), systemic sclerosis, Sjōgren Syndrome, and mixed connective tissue disease. Several investigators reported that ANA also occur in the serum of cancer patients (Abu-Shakra et al. 2001; Tan 2012; Vlagea et al. 2018), and the possibility that these autoantibodies may be related to DNA damage and cancer etiology was proposed (Noble et al. 2016; Vlagea et al. 2018). However, the plethora of different autoantibody specificities and challenges in their detection, plus inconsistencies with different cancer types, has made it difficult to test this hypothesis. A standardized method of ANA detection, the HEp-2000 indirect immunofluorescence test, was employed due to its reliability in detecting a wide range of autoantibodies, particularly in asbestos-exposed populations. The ALBIA method was also utilized to detect specific autoantibody targets associated in general with ANA in systemic autoimmune diseases (SAID), including those associated with amphibole exposure (Diegel et al. 2018).
Human Epithelial Type-2 Cell Image Classification Using an Artificial Neural Network with Hybrid Descriptors
Published in IETE Journal of Research, 2020
B. S. Divya, Kamalraj Subramaniam, H.R. Nanjundaswamy
The immune system detects a wide range of pathogens, which cause diseases. Each pathogen has a unique antigen on its surface. Antigen induces immune response to produce antibodies in the host to fight against pathogens. The immune system malfunctions by confusing the normal healthy tissues for the pathogens and fights against the normal healthy tissues by generating antibodies, thus causing damages. This condition is known as autoimmune disease. Antinuclear antibodies (ANA) are autoantibodies generated against own healthy cell nucleus causing autoimmune disease [1]. The likely developing autoimmune diseases are lupus, scleroderma, Sjögren’s syndrome, polymyositis/dermatomyositis, mixed connective tissue disease, drug-induced lupus, and autoimmune hepatitis [2].