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The Immune System in Cutaneous Disease: the Search for a Mouse Model of the Immunopathology of Psoriasis
Published in John P. Sundberg, Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
Susan F. Grammer, J. Wayne Streilein
Classical cell-mediated cytotoxicity is involved in delayed-type hypersensitivity, tumor rejection, graft rejection, viral clearance, autoimmune disease, contact hypersensitivity, and responses to intracellular organisms. Various skin cells can become targets of immunologic cellular cytotoxicity.27 The basal KC appears directly damaged in lupus erythematosus, lichen planus, contact dermatitis, and erythema multiforme. The differentiated KC is damaged in the above diseases, as well as pemphigus vulgaris, graft vs. host disease, and atopic dermatitis. Melanocytes are targets in depigmenting disorders, such as vitiligo and post-inflammatory hypopigmentation. Langerhans cells, circulating dermal leukocytes, and dermal macrophages may be targets in some diseases, but documentation has so far been difficult. In some diseases, especially the blistering diseases, the target may be structural proteins of the basement membrane zone rather than cells. Dermal fibroblasts may be targeted in fibrotic diseases, and endothelial cells in the dermis or subcutaneous tissue may be targets in vasculitis, scleroderma, and erythematosus multiforme.
Biology of the Hair and Skin
Published in Randy Schueller, Perry Romanowski, Conditioning Agents for Hair and Skin, 2020
The zone between the epidermis and the underlying dermis is referred to as the basement membrane zone or the epidermal-dermal junction (11). Below this lies the dermis, which is a moderately dense fibroelastic connective tissue composed of collagen fibers, elastic fibers, and an interfibrillar gel of glycosaminoglycans. Collagen is synthesized by the dermal fibroblasts and is responsible for the strength and 77% of the fat free dry weight of the skin. Interspersed between the collagen bundles is a network of elastic fibers that allow the skin to resist and recover following mechanical deformation (12).
Pregnancy-Related Protein Concentrations and Hormone Levels in Trophoblastic Diseases
Published in Gábor N. Than, Hans Bohn, Dénes G. Szabó, Advances in Pregnancy-Related Protein Research, 2020
Fay et al.60 discovered two more antigens of fetal origin like AFP; both FA-1 and FA-2 appear in significant quantity in amniotic fluid samples and fetal serum from the second or third trimester. Neither is identifiable from maternal serum, decidua, or fetal membranes. Third-trimester trophoblastic cells contain FA-1, but not FA-2.61 The latter was found to be present in the lamina densa/sublamina densa region of the basement membrane zone in adult as well as in fetal skin.62 Similar to AFP, FA-2 is unlikely to be of significance in trophoblastic diseases, and researchers have published no findings with respect to FA-1 in this regard.
Nanotechnology-based formulations toward the improved topical delivery of anti-acne active ingredients
Published in Expert Opinion on Drug Delivery, 2021
Ana Cláudia Paiva-Santos, Filipa Mascarenhas-Melo, Sara Cabanas Coimbra, Kiran D. Pawar, Diana Peixoto, Raquel Chá-Chá, André RTS Araujo, Célia Cabral, Selmo Pinto, Francisco Veiga
The basement membrane zone of the skin, located between the epidermis and dermis, is lined with basal stem cells that change into sebaceous cells or keratinocytes responsible for sebum production and hair growth. The proliferation of these cells is regulated by hormones, specifically androgens [2]. When hormonal dysregulation events occur, an abnormal over-keratinization triggers several pathogenic processes that affect the PSU, activating immunological host reactions and causing inflammation, contributing to the development of acne-associated lesions [2,6,7]. During these events, the colonization and proliferation of commensal gram-positive bacteria, such as Staphylococcus aureus (S. aureus), Staphylococcus epidermidis (S. epidermidis) and Cutibacterium acnes (C. acnes), also known as Propionibacterium acnes (P. acnes) become favorable [8,9].
Pathophysiology, diagnosis, and pharmacological treatment of prurigo nodularis
Published in Expert Review of Clinical Pharmacology, 2021
Kyle A. Williams, Youkyung S. Roh, Isabelle Brown, Nishadh Sutaria, Pegah Bakhshi, Justin Choi, Sylvie Gabriel, Rajeev Chavda, Shawn G. Kwatra
There are several dermatologic conditions that can mimic PN that should be considered when evaluating patients. Pemphigoid nodularis, a rare variant of bullous pemphigoid, is characterized by pruritic nodules, papules, or plaques that mimic PN both clinically and histologically [44]. It may be especially challenging to distinguish the two conditions as they tend to affect populations of similar age groups (50s to 60s) with female predominance [44]. Additionally, pemphigoid nodularis can arise in the context of other chronic pruritic conditions, including PN [45–48], so it is helpful to be cognizant of this diagnosis in patients with persistent pruritus, even in established PN patients. Compared to PN, however, pemphigoid nodularis often presents with larger plaques with areas of central erosion, ulceration, and/or blistering traditionally seen in bullous diseases [4,49]. A pathognomonic feature is seen on biopsy, which shows subepidermal clefting, and linear deposition of IgG and C3 along the basement membrane zone on direct immunofluorescence (DIF) staining, which is absent in PN. Patients also have circulating autoantibodies against the basement membrane zone [50].
Leading edge: emerging drug, cell, and gene therapies for junctional epidermolysis bullosa
Published in Expert Opinion on Biological Therapy, 2020
Allison R. Keith, Kirk Twaroski, Christen L. Ebens, Jakub Tolar
The basement membrane zone (BMZ) of the skin is studded with hemidesmosomes (HDs), which act as biological ‘rivets’ to bind the upper epidermis and lower dermis. The major proteins that comprise HDs are LM332, C17, integrin α6β4, and Type VII collagen (C7) anchoring fibrils (Figure 1(a)). Function-altering mutations in any of these components lead to various forms of EB. Adhesion proteins and receptors are concentrated at the HDs of the BMZ, allowing for crosstalk between the skin layers and imparting mechanical strength and regenerative cues that allow the skin to function as a cohesive structure [19]. LM332 is an ECM protein that interacts with integrin α6β4 on the basal surface of epidermal keratinocytes to convey external mechanical inputs, in addition to binding C7 to maintain adhesion to the underlying dermis. C17 interacts with extracellular LM332 and the intracellular domain of integrin β4 to stabilize the HDs [20]. The innate dysfunction of the ECM in JEB impacts both the skin barrier function and its resident immune population [21]. The ECM serves as a critical attachment site for immune cells, such as mast cells and developing thymocytes [21–24].