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Moderate-to-severe systemic lupus erythematosus (SLE) is characterized by extensive autoantibody deposition and persistent autoinflammation. As the existing animal models are limited in accurately reproducing the pathological characteristics of human SLE, we introduced a novel animal model simulating multi-organ autoinflammation through intra-organ injections. The model closely mimicked key features of SLE, including IgG deposition, inflammation, and tissue damage. The model could be used to assess the roles of IgG, immune cells, cytokines, and Fc gamma receptor (FcγR) in the pathogenesis of autoinflammation. The results obtained from this model could be confirmed by lupus MRL/ lpr mice. The review suggested that the diagnostic criteria should be reconsidered to incorporate IgG deposition in tissues and highlighted the limitations of current T-cell and B-cell-focused treatments. To summarize, the IgG deposition model can be used to investigate the pathogenesis and treatment of multi-organ tissue damage associated with SLE. • Introduction of a novel animal model: a new animal model mimicing the pathogenesis of lupus autoantibodies IgG-induced organ-tissue damage. • Comprehensive Exploration and Validation of New Model: The roles of lupus autoantibody IgG, immune cells, cytokines and FcγR in organ tissue inflammation were investigated by using this new model. Confirmation of the results from the new model using lupus-prone MRL/lpr mice. • Implications for SLE Research and Treatment: Importance and convenience of the IgG deposition model in investigating the pathogenesis of SLE and its potential for developing targeted therapies. • This paper significantly contributes to the understanding of SLE pathogenesis by introducing a novel animal model that accurately replicates key aspects of the disease, providing a platform for more effective therapeutic exploration and diagnostic considerations. [ABSTRACT FROM AUTHOR]

This paper summarizes and reviews the mechanisms of action and data concerning efficacy of recommended treatments as well as other treatments that have been tested, independently of the outcomes, in the management of chronic spontaneous urticaria. Due to the central role of mast cells, basophils and histamine in the pathophysiology of this disease, H 1 -antihistamines remain the first-line treatment. However, current knowledge about this complex disease, also recognizes an important role for T lymphocytes, B lymphocytes, and autoantibodies. Implications of these others mediators thus provide further targets for treatment. Indeed, agents previously used to treat other autoimmune and inflammatory diseases, have demonstrated efficacy in chronic spontaneous urticaria and are therefore potential therapeutic alternatives for antihistamine unresponsive patients. [ABSTRACT FROM AUTHOR]

This paper is a review, personal memoir, a tribute to Henry Kunkel, and a critique regarding laboratory tests used for the evaluation, diagnosis, and understanding Autoimmune Rheumatic Diseases, in particular systemic lupus erythematosus (SLE). [ABSTRACT FROM AUTHOR]

Children with idiopathic nephrotic syndrome (INS) usually have podocyte injury, and recent studies suggest a B cell dysfunction in INS. Therefore, this study attempts to screen and identify the podocyte autoantibodies in patients. Two-dimensional electrophoresis and mass spectrometry were used to screen and identify the pathogenic podocyte autoantibodies in children with INS. The positive rate, expression pattern, and clinical correlation of these podocyte autoantibodies in children with INS were determined by clinical study. At least 66% of INS children have podocyte autoantibodies. Seven podocyte autoantibodies closely related to INS were screened and identified for the first time in this study. These podocyte autoantibodies are positively correlated with proteinuria, and its titer will decrease rapidly after effective treatment. In this study, a group of new disease subgroup-"autoimmune podocytes" were identified by podocyte autoantibodies. This paper used 2D electrophoresis combined with mass spectrometry to screen and identify podocyte autoantibodies specific to primary nephrotic syndrome. The protein microarray was used for clinical validation. Finally, seven podocytes autoantibodies specific to the serum of primary nephrotic syndrome were identified. These antibodies were positively correlated with urinary protein levels and efficacy. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract: Although autoantibodies against the α1-adrenergic receptor which had been found in hypertensive patients had agonist-like activity as phenylephrine, the effects of these antibodies on cardiac remodeling have not been known. In this paper, the models with agonist-like activity of antibodies to α1-adrenergic receptor were made by immunized Wistar rats using synthesized peptides of α1A-adrenergic receptor and raised for 1 year, and the excited antibodies against the α1-adrenergic receptor which could elevate the free Ca2+ in isolated adult rat cardiomyocytes had been existed throughout the experiments after immunization. In immunized rats, despite that systolic blood pressure (SBP) had no difference with normal control, the hypertrophy of heart and cardiomyocytes was observed, the collagen deposition in heart interstitium increased, and c-jun expression and matrix metalloproteinase (MMP)-2 mRNA expression and activity in heart had increased. The results suggested that antibodies against the α1-adrenergic receptor could induce cardiac remodeling and maybe play a particular role in hypertension. [Copyright &y& Elsevier]

Abstract Chronic fatigue syndrome, postural orthostatic tachycardia syndrome, complex regional pain syndrome and silicone implant incompatibility syndrome are a subject of debate among clinicians and researchers. Both the pathogenesis and treatment of these disorders require further study. In this paper we summarize the evidence regarding the role of autoimmunity in these four syndromes with respect to immunogenetics, autoimmune co-morbidities, alteration in immune cell subsets, production of autoantibodies and presentation in animal models. These syndromes could be incorporated in a new concept of autoimmune neurosensory dysautonomia with the common denominators of autoantibodies against G-protein coupled receptors and small fiber neuropathy. Sjogren's syndrome, which is a classical autoimmune disease, could serve as a disease model, illustrating the concept. Development of this concept aims to identify an apparently autoimmune subgroup of the disputable disorders, addressed in the review, which may most benefit from the immunotherapy. • Autoimmune aspects of CFS, POTS, CRPS and SIIS are discussed. • The common denominators of anti-GPCR AAb and SFN are identified for these syndromes. • A new concept of autoimmune neurosensory dysautonomia is suggested. • Sjogren's syndrome can illustrate the suggested concept. [ABSTRACT FROM AUTHOR]