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The Viruses
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
of immune complexes and complement on the infected cells. Persistent expression of viral antigen by infected cells may also induce cell mediated immune responses and delayed-type hypersensitivity reactions leading to chronic inflammation and tissue damage at the site of infection. A number of viral diseases and their etiologic agents are summarized in Table 16.2. In this table, diseases are grouped by whether the causative virus produces acute, persistent or chronic infection. Various viral diseases are described in a later section of this chapter.
Introduction to dermatological diagnosis
Published in Richard Ashton, Barbara Leppard, Differential Diagnosis in Dermatology, 2021
Richard Ashton, Barbara Leppard
If the diagnosis is in doubt an ellipse of skin can be taken through the edge of the lesion, so that both normal and abnormal skin are included in the specimen. It should include epidermis, dermis and fat. Immune complexes can be identified by immunofluorescence. The sample needs to be sent to the laboratory in Michel's medium. A ‘punch biopsy’ takes a 3–6 mm core of tissue, but this technique produces only a limited sample. It is useful for diagnosis of skin tumours where full excision is not possible. It should not be used for histological examination of inflammatory dermatoses. If a skin tumour is present, the whole lesion should be excised if possible as an ellipse so that the wound can be sewn up in a straight line. A punch biopsy should only be taken if the diagnosis is in doubt, or the lesion too large to remove routinely.
An Overview of Allergic Contact Dermatitis from Topical Drugs
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
There are various special and atypical forms and manifestations of allergic contact dermatitis. Well-known are erythema multiforme-like eruptions. These are not well-defined and are usually based on the morphological interpretation of the investigator. However, besides the occasional target-like lesions, the morphology (with urticarial papules and plaques), clinical course and history of erythema multiforme-like eruptions of contact allergy are not characteristic of classical erythema multiforme. They also lack the histopathology of ‘real’ erythema multiforme. Some authors therefore prefer the term ‘urticarial papular and plaque eruptions’. The exact mechanism is unknown, but allergic immune complexes are thought to play a role (153). Topical drugs that have caused EM-like allergic contact dermatitis are shown in table 2.3.
TRYBE®: an Fc-free antibody format with three monovalent targeting arms engineered for long in vivo half-life
Published in mAbs, 2023
Emma Davé, Oliver Durrant, Neha Dhami, Joanne Compson, Janice Broadbridge, Sophie Archer, Asher Maroof, Kevin Whale, Karelle Menochet, Pierre Bonnaillie, Emily Barry, Gavin Wild, Claude Peerboom, Pallavi Bhatta, Mark Ellis, Matthew Hinchliffe, David P. Humphreys, Sam P. Heywood
The TrYbe® format was specifically conceived to facilitate monovalent target binding in an Fc-free molecule. The value of this was highlighted when targeting multivalent antigens such as TNF and IL-17A. TrYbes® formed vastly smaller antibody-antigen complexes in vitro compared to comparator bivalent, bispecific IgG-based formats. The formation of small immune complexes is a natural consequence of antibody-antigen engagement in clinical settings. However, potentially serious issues such as immunogenicity or immune complex disorders have been reported, the former due to clearance via antigen presenting cells and the latter arising from unsuccessful clearance of immune complexes from circulation and their subsequent deposition in tissues and organs.11,82,83 These disorders can be aggravated by Fc-containing complexes and aberrant activation of Fc effector functionalities including complement activation. Our studies support previous reports,10,11 which conclude that both antigen and antibody valency, and the ratio of antigen to antibody are important factors that contribute to the formation of these complexes in vitro. This was shown to be further complicated when considered in the context of bispecific targeting and underlies the importance to carefully consider not only the mode of action of the antibody but also properties of the targeted antigens along with the design of the therapeutic molecule. By being monovalent and Fc-free, the TrYbe® is favorably placed in this context to minimize potential risks.
Diminished LAG3+ B cells correlate with exacerbated rheumatoid arthritis
Published in Annals of Medicine, 2023
Suiyuan Hu, Yuting Tao, Fanlei Hu, Xu Liu
B cells play a vital role in the pathogenesis of RA [1]. Naive B cells are activated and differentiate into plasma cells which produce autoantibodies like rheumatoid factor and anti-citrullinated protein antibody (ACPA). These autoantibodies form immune complexes (IC) and trigger perpetual inflammation. Additionally, B cells can produce proinflammatory factors such as IL-6, which drives autoimmune reactions [2]. Thus, various B-cell-targeting drugs have been developed, such as rituximab, a chimeric murine/human monoclonal CD20 antibody. While its effectiveness has been verified by a phase III clinical trial, only 30% of RA patients treated with rituximab showed an American College of Rheumatology 50% improvement criteria (ACR50) response at 24 weeks [3]. One of the underlying reasons might be the reduction of regulatory B (Breg) cells in general B cell depletion therapy.
Enhanced immunogenic potential of cancer immunotherapy antibodies in human IgG1 transgenic mice
Published in mAbs, 2022
Jerome Egli, Stefan Heiler, Felix Weber, Guido Steiner, Timo Schwandt, Katharine Bray-French, Christian Klein, Sebastian Fenn, Gregor P. Lotz, Eugenia Opolka-Hoffmann, Thomas E. Kraft, Laetitia Petersen, Rebecca Moser, Jonathan DeGeer, Michel Siegel, Daniela Finke, Juliana Bessa, Antonio Iglesias
Immune complexes were prepared and characterized as described previously.41 In short, a mixture containing 2 mg/ml CEA-IgG and 3 mg/ml monoclonal mIgG2a anti-idiotype antibody was prepared in histidine buffer (20 mM histidine, 140 mM NaCl, pH 6.0) and incubated for 1 h at room temperature on a shaker at 500 rpm. The ICs were characterized as previously described.41 In brief, a Waters XBridge Protein BEH SEC Guard Column, 450 Å, 3.5 μm, 7.8 mm × 30 mm and a XBridge Protein BEH SEC Column, 450 Å, 3.5 μm, 7.8 mm × 300 mm were used in a Dionax UltiMate 3000 system from Thermo Fisher Scientific GmbH (ultraviolet (UV) detector MWD-3000, auto sampler, automated fraction collector). 20 μl of centrifuged dosing solutions were injected for analysis. Phosphate-buffered saline (PBS) with 5% ethanol (v/v) was used as running buffer with a flow rate of 0.5 ml/min. Online UV detection was performed at 280 nm.