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Systemic Lupus Erythematosus
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Vaneet K. Sandhu, Neha V. Chiruvolu, Daniel J. Wallace
Despite the 2019 EULAR/ACR criteria heavily emphasizing ANA as the entry criterion for the diagnosis of SLE, a positive ANA can be found in up to 30% of the general population and in other autoimmune conditions such as scleroderma, rheumatoid arthritis, Sjögren’s syndrome, and mixed connective tissue disease. ANA has been heavily criticized for its poor specificity,10 and there is emerging investigation into autoantigen arrays. Proteome microarray-based technology has been utilized for years to identify biomarkers in many diseases. Autoantigen arrays are used to screen and identify interactions between antigens and antibodies on a large scale.11 One of the benefits of this technology is that antibodies can be detected at a level of less than 1 ng/ml. Small samples, close to 1–2 microliters, can be obtained from serum, body fluids, or cell culture supernatant. Antibodies that bind to corresponding antigens on the array are detected using a fluorophore conjugate of second antibodies against different isotypes of autoantibodies (IgG, IgM, IGA, IgE). One of the marvels of autoantibody arrays is their capacity to detect hundreds of thousands of autoantibodies quantitatively and even prior to clinical onset of disease, thereby serving as an early diagnostic tool. Furthermore, quantification of antibodies may be helpful in monitoring disease activity and response to treatment. Data obtained from these arrays have demonstrated greater sensitivity in comparison to enzyme-linked immunosorbent assay (ELISA).12
AI and Autoimmunity
Published in Louis J. Catania, AI for Immunology, 2021
No single laboratory test can diagnose autoimmune diseases. It requires a physical examination to assess signs and symptoms with a combination of lab tests. The antinuclear antibody test (ANA) is often one of the first tests used when symptoms suggest an autoimmune disease. A positive ANA test suggests the potential presence of autoimmune disease, but it does not confirm exactly which one or even if one is present for certain. Other tests look for specific autoantibodies produced in certain autoimmune diseases. The bottom line is laboratory diagnosis is non-specific and can only assist in the symptoms and other tests to confirm the diagnosis.40
Immune Testing in Recurrent Pregnancy Loss*
Published in Howard J.A. Carp, Recurrent Pregnancy Loss, 2020
Jeffrey Braverman, Darren Ritsick, Nadera Mansouri-Attia
Additional useful serological markers for autoimmune disease include thyroid autoantibodies (anti-TPO, anti-thyroglobulin, anti-TSH receptor), antinuclear antibodies (ANAs), rheumatoid factor, and anti-CCP antibodies. In addition to an ANA screen for titer and staining pattern, testing for specific species of ANA (i.e., ANA-Sm, ANA-Ro, ANA-La, ANA-dsDNA, etc.) can be useful to more specifically define underlying autoimmune conditions.
The onset of de novo autoantibodies in healthcare workers after mRNA based anti-SARS-CoV-2 vaccines: a single centre prospective follow-up study
Published in Autoimmunity, 2023
M.C Sacchi, C. Pelazza, M. Bertolotti, L. Agatea, P. De Gaspari, S. Tamiazzo, D. Ielo, P. Stobbione, M. Grappiolo, T. Bolgeo, P. Novel, M.M Ciriello, A. Maconi
At T1 and T2, five ANA patterns were considered: homogeneous; speckled; cytoplasmatic; nucleolar; other (e.g. midbody, centrosomes, spindle poles). At T1, the homogeneous pattern was observed in 5/6 samples, the speckled in 4/6 and the cytoplasmatic in 1/6 (Figure 3 A, D). At T2, the type of pattern observed increased: homogeneous was observed in 12/21, speckled in 6/21, nucleolar in 2/21, cytoplasmic in 1/21 and other patterns in 7/21 (Figure 3 C, E). The most common pattern was the homogeneous pattern, although one patient had more than one pattern. The homogeneous pattern is usually associated with the presence of anti dsDNA, nucleosomes, and histones antibodies. All the T2 homogeneous positive samples were tested with a confirmatory assay and resulted negative for these autoantibodies. We also evaluated the pattern distribution, which showed no statistical significance both within each time point (T1 and T2; p-value: 0,11642) and between them (T1 versus T2; p-value: 0,07364). In terms of antibody titres, none of the patterns analysed showed a statistical increase from T1 to T2.
Posterior Scleritis Following COVID-19 Vaccination: A Case Report
Published in Ocular Immunology and Inflammation, 2023
The pathogenesis of vaccine-associated ocular adverse events is unknown. We postulate our patient’s posterior scleritis was an immune-mediated reaction. The immunogenicity of the ChAdOx1 vaccine has been demonstrated in vaccine-induced immune thrombotic thrombocytopenia (VITT).11 Here, the generation of autoantibodies against platelet factor 4 (PF4) causes widespread consumption coagulation and venous thrombotic events. We thought, as seen in our patient, an elevated ANA titre may be a speculative sign of an autoimmune response following vaccination. We excluded dsDNA and ENAs as potential target antigens. Furthermore, the negativisation of ANA following systemic corticosteroid treatment supports a transient immune event. The precise mechanism(s) by which the ChAdOx1 vaccine is able to induce autoantibody production is yet to be determined. Close observation of autoantibodies following vaccination should be looked for in longitudinal studies to corroborate our findings.
The spectrum of renal diseases with lupus-like features: a single-center study
Published in Renal Failure, 2022
Maliha Ahmed, Tanzy Love, Catherine Moore, Thu H. Le, Jerome Jean-Gilles, Bruce Goldman, Hae Yoon Grace Choung
Because of the strong pathologic similarities with LN, some speculate that both LN and LLN share similar patho-mechanisms. Autoantibody formation and resultant inflammation in SLE has been hypothesized to be related to dysregulated apoptosis and poor clearance of apoptotic debris, which subsequently exposes cryptic self-antigens to an abnormal immune response leading to self-directed antibodies and defective clearance of immune complexes [25]. Some authors have suggested that the full-house immune deposition seen in LN may be due to the pronounced polyclonal B-cell activation and immune response in the setting of these mechanisms and that LLN could very well be a manifestation of a similar aberrant process [7]. This process may also explain why some cases with delayed SLE presentations are ANA-negative initially. Auto-antibodies directed to other components of nuclear material, such as nucleosomes or DNA-histone complex have been proposed as potential antigenic factors LN [26]. Autoantibodies to nucleosomes have been found to either bind to deposited nucleosomes or cross-react with glomerular constituents, and its formation appears to precede anti-dsDNA or anti-histone autoantibodies [27,28]. Thus tests for specific autoantibodies against a particular nuclear component may be positive while ANA is negative [29]. Furthermore, it is conceivable that some LLN patients who do not present with serological evidence of SLE even after many years of follow-up may have an undetectable autoantibody to a specific component of nuclear material for which a test is unavailable.