By B.J. Nickoloff, F.O. Nestle, A.N. Theofilopoulos
The surface, being the biggest organ of the physique, is consistently attacked by means of a various array of pathogenic brokers together with micro organism, viruses and fungi; it additionally suffers from sun harm and large fluctuations in temperature and humidity. In a few members, the immune process, which often bargains defense opposed to deadly exterior attacks, can malfunction and reason power irritation within the absence of a identified pathogen, leading to a bunch of problems labeled as autoimmune dermis ailments. This quantity features a sequence of nineteen evaluation articles on a variety of autoimmune sickness approaches within the dermis. that includes issues of humoral in addition to mobile immunity, it covers allergic touch dermatitis, poisonous epidermal necrolysis, psoriasis, atopic dermatitis, cutaneous lupus erythematosus, bullous pemphigoid, pemphigus foliaceus, lichen planus, vitiligo, scleroderma, alopecia areata and dermatomyositis.For those ailments, the most recent insights into their etiology and pathophysiology in addition to healing ideas are offered via specialists within the fields of dermatology, genetics, immunology and pathology. moreover, overviews of the outside as an lively immune organ and of the immune privilege of the outside are integrated. entire and updated, this e-book is suggested for simple and medical researchers, allergists, immunologists, dermatologists, internists and a person attracted to autoimmunity.
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Additional info for Dermatologic Immunity
Human anagen VI scalp HFs show CD4ϩ T cells extremely rarely, and a CD8ϩ lymphocyte is almost never caught trafficking through the proximal follicle epithelium . Like the other well-defined immune-privileged tissues, the hair bulb is characterized by the absence of lymphatic drainage pathway and the presence of a special extracellular matrix barrier around the HF, both of these conditions may contribute to hinder immune cell trafficking [43, 47]. Importantly, anagen hair bulbs in mice and man express potent immunosuppressants such as TGF-␤1 [39, 48], ACTH [49, 50] and ␣-MSH [50–54].
Eur J Immunol 1997;27:3031–3038. Hauser C: Cultured epidermal Langerhans cells activate effector T cells for contact sensitivity. J Invest Dermatol 1990;95:436–440. Cumberbatch M, Fielding I, Kimber I: Modulation of epidermal Langerhans’ cell frequency by tumour necrosis factor-␣. Immunology 1994;81:395–401. Cumberbatch M, Kimber I: Dermal tumour necrosis factor-␣ induces dendritic cell migration to draining lymph nodes, and possibly provides one stimulus for Langerhans’ cell migration. Immunology 1992;75:257–263.
36] and Hofmann et al. ). human terminal HFs. These authors found that MHC class I molecules are present on the surface of epidermal basal and spinous layer keratinocytes, and on the outer root sheath (ORS) epithelium in the infundibulum of the HF. In contrast, dermal papilla, proximal ORS and inner root sheath (IRS) showed negative MHC class I expression. Ia-like, antigen-positive dendritic cells are also observed rarely in deep portion (around the proximal HFs). On the other hand, distal ORS shows strong positive expression of MHC class I and many Ia-like, antigen-positive dendritic cells.