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Native And Acquired Resistance To Infection With Cryptococcus Neoformans
Published in Hans H. Gadebusch, Phagocytes and Cellular Immunity, 2020
A cryptococcocidal substance found in the normal serum of man and other mammals but absent in pigeon serum51 has been described by Allen48 and later by Baum and Artis,49 Gadebusch,50 and by Igel and Bolande.36 This material is heat-stable (56°C for 30 min) and not related to properdin or complement-dependent systems. While some have suggested52 that the iron-binding β-globulin, transferrin, is responsible for this activity because reversal could be accomplished by the addition of FeCl3, others were unable to demonstrate deleterious effects upon the organism by rabbit transferrin, either iron-free or iron-saturated.53 The isolation and purification from human platelets of plakin, a cationic protein known to possess cryptococcocidal activity in vitro,42 and the demonstration that antibody to purified β-lysin can inactivate plakin and vice versa54 suggests that the anticryptococcal substance in serum is similar to, if not identical with, /Mysin and has its origin in platelets. The role of this substance upon cryptococci while in transit in the blood stream is probably minimal and at most inhibitory to the fungus. The role(s) and presumed mechanism of action in other sites will be discussed in Section IV.
Paraneoplastic pemphigus
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
The major pathogenic mechanisms of PNP include the following: Unmasking antigen targets: The neoplastic process induces an autoimmune disorder in which both humoral and cell-mediated immunity are involved. Cell-mediated lichenoid interface dermatitis induced by the tumor uncovers previously hidden epithelial antigens through epitope spreading [6].Antigenic mimicry: Cross-reactivity occurs between antibodies directed against tumor cells and epithelial antigens. First, damage to the cell membrane induced by antibodies directed against transmembrane desmoglein-3 initiates acantholysis and subsequently provides access to intracellular proteins. Antibodies to intracellular plakin proteins produce unique features of PNP like dyskeratosis.Cytokine dysregulation: Dysregulation of cytokine production is induced by the tumor cells with massive secretion of IL-6. It promotes maturation of lymphocytes, activation of cytotoxic T cells, and antibody production [7].
Autoimmune blistering diseases: promising agents in clinical trials
Published in Expert Opinion on Investigational Drugs, 2023
Henning Olbrich, Christian D. Sadik, Enno Schmidt
Pemphigus diseases are characterized by intraepidermal cleft formation induced by autoantibodies against desmosomal structures. The main subtypes of pemphigus are pemphigus vulgaris (PV) and pemphigus foliaceus (PF); paraneoplastic pemphigus (PNP) and IgA pemphigus are extremely rare [1,2]. PV is the most frequent subtype at an incidence of 1–10 per million per year with middle-aged persons affected most commonly [25]. It presents with painful erosions and ulcers of mucous membranes, mostly in the oral cavity, as well as flaccid blisters and erosions of the skin. PF exclusively involves the skin and shows puff-pastry-like scaling and erosions mainly in seborrheic areas, whilst PNP is characterized by severe mucositis affecting oral, ocular, anogenital, bronchopulmonary, and gastrointestinal mucosae besides skin [26]. DIF in PV, PF, and PNP shows intercellular deposits of IgG, complement C3 and more rarely IgA within the epidermis. Target antigens are desmoglein (Dsg)-3 and -1 in PV, Dsg-1 in PF and various desmosomal and plakin molecules in PNP including Dsg-1 and -3, desmocollins, envo-, peri-, and desmoplakin, plectin, BP230 [27–29] and α2-macroglobulin-like 1 protein [30].
Urinary proteomics for kidney dysfunction: insights and trends
Published in Expert Review of Proteomics, 2021
As detailed above, early detection of graft injury is key to maintaining long-term graft function. In an attempt to reveal early molecular processes of transplant biology, proteomics of uEVs isolated from living donors and transplant recipients was performed [108]. The study identified uEV protein signatures and cellular processes involved in both early response and longer-term graft adaptation. Furthermore, a putative prognostic marker of future allograft function, phosphoenol pyruvate carboxykinase (PCK2), was uncovered. In another study, proteomic characterization of uEVs from kidney-transplanted patients treated with calcineurin inhibitors (for immunosuppression) suggested important roles of uroplakin and plakin family proteins in chronic calcineurin inhibitor toxicity [109].
Dipeptidyl peptidase IV inhibitor-associated bullous pemphigoid: a recently recognized autoimmune blistering disease with unique clinical, immunological and genetic characteristics
Published in Immunological Medicine, 2019
BP autoantibodies target two epidermal autoantigens: BP180 and BP230. Both are hemidesmosomal components in basal keratinocytes (Figure 2(A)) [1,2]. BP180 is a 180-kD type-II transmembrane collagen whose amino (N) and carboxyl (C) termini are located in the cytoplasm and extracellular matrix, respectively (Figure 2(A)). In contrast, BP230 is a 230-kD intracytoplasmic plakin family protein. The majority of BP autoantibodies target the juxtamembranous extracellular NC16A domain of BP180 (Figure 2(B)) [12], and the serum level of anti-BP180 NC16A usually correlates with the disease severity and clinical course [13,14]. The passive transfer of anti-BP180 NC16A autoantibodies into BP180-humanized transgenic mice has revealed that the autoantibodies cause pathogenic skin fragility [3,4]. Regional BP skin usually shows activated complements at the DEJ, suggesting that a complement-mediated inflammatory mechanism plays a role in blister formation. In addition, anti-BP180 NC16A autoantibodies have been experimentally shown to have pathogenicity in a complement-independent manner by depleting BP180 expression in basal keratinocytes [15,16]. This notion is consistent with the fact that BP may not induce complement activation at the DEJ, probably due to complement non-fixing IgG4-class anti-BP180 autoantibodies [17]. Furthermore, IgE-class autoantibodies to BP180 may be associated with the formation of itchy urticarial erythema and lesional eosinophilic infiltration [18]. Whereas the pathological roles of anti-BP180 autoantibodies have been elucidated, those of anti-BP230 autoantibodies have not.