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Hematopoietic Stem Cell Transplantation in Patients with Autoimmune Bullous Skin Disorders
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Pemphigus vulgaris, like all diseases in the pemphigus group, is pathologically characterized by intraepidermal suprabasal acantholytic blisters with detachment of adjacent epidermal keratinocytes. The diagnosis of pemphigus is confirmed by direct immunofluorescence, which shows IgG deposited on the surface of keratinocytes in and around lesions. Anti-desmoglein antibodies can also be detected using ELISA methods in 80-90% of patients.
A comprehensive summary of disease variants implicated in metal allergy
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Although the causes of these disorders remain largely unclear, it has become recognized that some exposure conditions might promote the development of autoantibodies to epidermal proteins. For example, some drugs have been associated with the induction of structural changes in the epidermis that lead to sensitization. Although quite uncommon, dermal contact with metals was also implicated in similar mechanisms and subsequent development of pemphigus or pemphigoid in susceptible individuals. Accordingly, two reports described the emergence of pemphigus vulgaris in subjects with Ni-containing dental prostheses (Stransky 1998; Thongprasom et al. 2011). The extended duration of contact with the oral mucosa was suggested to result in the formation of novel antigens and subsequent sensitization, leading to pemphigus-like lesions in and around the mouth. Gold was also associated with the potential to initiate both pemphigus and pemphigoid in subjects receiving systemic Au therapy (Iveson et al. 1977; Lo Schiavo et al. 2008). Paradoxically, one of the indications for gold salt therapy is pemphigus (Faa et al. 2018). While some patients achieve relief from autoimmune symptoms following treatment, others subsequently develop autoreactive antibodies. This response was suggested to result from similar mechanisms known to occur in cases of drug-induced pemphigoid, wherein a drug triggers conformational changes in host proteins of the skin and subsequent sensitization of the patient to gold/host protein complexes (Van Der Voet 2010).
Genetic variants affecting chemical mediated skin immunotoxicity
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Isisdoris Rodrigues de Souza, Patrícia Savio de Araujo-Souza, Daniela Morais Leme
The majority of mature B cells reside within lymphoid follicles of the spleen and lymph nodes and it is still unclear if B cells are present in the skin as resident cells (LeBien and Tedder 2008; Nguyen and Soulika 2019). As to T lymphocytes, B lymphocytes move to the skin tissue via CLA, and it may also be dependent upon the CCL20-CCR6 axis (Nguyen and Soulika 2019). These cells are frequently associated with delayed-type hypersensitivity reactions and produce allergen-specific IgM antibodies. The formation of these immune complexes might lead to activation of the complement cascade, resulting in T cell recruitment to the affected skin site (Tsuji et al. 2002). In addition, regulatory B cells suppress autoreactive lymphocyte activation through IL-10 production. These cells may play suppressive role in autoimmune skin diseases such as Pemphigus vulgaris and imiquimod-induced murine psoriasis model (Tavakolpour 2018; Yanaba et al. 2013).