The Experts below are selected from a list of 45 Experts worldwide ranked by ideXlab platform
Hideo Yaoita - One of the best experts on this subject based on the ideXlab platform.
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different effects of Pemphigus Antibody and plasmin on the distribution of keratin intermediate filaments and desmoplakins between cultured oral and epidermal keratinocytes
Journal of Dermatological Science, 1992Co-Authors: Yoshinori Jinbu, Yasuo Kitajima, Shigeaki Koto, Yoko Akasaka, Hideo YaoitaAbstract:In order to clarify the molecular mechanism of blister formation in oral mucosa in Pemphigus vulgaris (PV) comparing with that in epidermis, we analyzed the effects of PV serum on the distribution of keratin intermediate filaments (KIFs) and desmoplakins in oral as well as epidermal cultured keratinocytes by immunofluorescence microscopy using anti-keratin and anti-desmoplakin I/II monoclonal antibodies. After incubation with PV serum for 96 h at 37 degrees C, clusters of anti-keratin positive dots were formed around the nucleus in some of the keratinocytes from normal gingiva and soft palate but not in keratinocytes from tongue and skin, and desmoplakins also changed their distribution from linear arrangement at cell-cell contacts to clusters of dots around the nucleus in gingiva but not in epidermal keratinocytes. The dotted structures similar to those induced by Pemphigus serum were formed also by incubation with human plasmin in gingival keratinocytes. However, no dot-formation of keratins was induced in these cells after incubation with trypsin. Furthermore, in epidermal keratinocytes, no keratin-dot formation was observed even after incubation with plasmin or trypsin. These results suggest that the dotted structures of KIFs caused by PV serum and plasmin might be a feature characteristic for the response of oral keratinocytes to PV serum and that there are some distinct differences in susceptibility to, and mode of, bulla formation between oral epithelium and epidermis.
Yoshinori Jinbu - One of the best experts on this subject based on the ideXlab platform.
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different effects of Pemphigus Antibody and plasmin on the distribution of keratin intermediate filaments and desmoplakins between cultured oral and epidermal keratinocytes
Journal of Dermatological Science, 1992Co-Authors: Yoshinori Jinbu, Yasuo Kitajima, Shigeaki Koto, Yoko Akasaka, Hideo YaoitaAbstract:In order to clarify the molecular mechanism of blister formation in oral mucosa in Pemphigus vulgaris (PV) comparing with that in epidermis, we analyzed the effects of PV serum on the distribution of keratin intermediate filaments (KIFs) and desmoplakins in oral as well as epidermal cultured keratinocytes by immunofluorescence microscopy using anti-keratin and anti-desmoplakin I/II monoclonal antibodies. After incubation with PV serum for 96 h at 37 degrees C, clusters of anti-keratin positive dots were formed around the nucleus in some of the keratinocytes from normal gingiva and soft palate but not in keratinocytes from tongue and skin, and desmoplakins also changed their distribution from linear arrangement at cell-cell contacts to clusters of dots around the nucleus in gingiva but not in epidermal keratinocytes. The dotted structures similar to those induced by Pemphigus serum were formed also by incubation with human plasmin in gingival keratinocytes. However, no dot-formation of keratins was induced in these cells after incubation with trypsin. Furthermore, in epidermal keratinocytes, no keratin-dot formation was observed even after incubation with plasmin or trypsin. These results suggest that the dotted structures of KIFs caused by PV serum and plasmin might be a feature characteristic for the response of oral keratinocytes to PV serum and that there are some distinct differences in susceptibility to, and mode of, bulla formation between oral epithelium and epidermis.
H. Tagami - One of the best experts on this subject based on the ideXlab platform.
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The role of complement-derived mediators in inflammatory skin diseases
Archives of Dermatological Research, 1992Co-Authors: H. TagamiAbstract:The complement system represents an important nonspecific skin defense mechanism. Its activation leads to the generation of products that not only help to maintain normal host defenses but also mediate inflammation and tissue injury. Proinflammatory products of complement include large fragments of C3 with opsonic and cell-stimulatory activities (C3b and C3bi), low molecular weight anaphylatoxins (C3a, C4a, and C5a), and membrane attack complex. Among them C5a or its degradation product C5a des Arg seems to be the most important mediator because it exerts a potent chemotactic effect on inflammatory cells. Intradermal administration of C5a anaphylatoxin induces skin changes quite similar to those observed in cutaneous hypersensititivy vasculitis that occurs through immune complex-mediated complement activation. Complement activation is involved in the pathogenesis of the inflammatory changes in autoimmune bullous dermatoses. In Pemphigus complement activation by Pemphigus Antibody in the epidermis seems to be responsible for the development of characteristic inflammatory changes termed eosinophilic spongiosis. In bullous pemphigoid (BP) interaction of basement membrane zone antigen and BP Antibody leads to complement activation that seems to be related to leukocytes lining the dermoepidermal junction. Resultant anaphylatoxins not only activate the infiltrating leukocytes but also induce mast cell degranulation which facilitates dermoepidermal separation and eosinophil infiltration. Similar complement activation seems to play a more direct role in the dermoepidermal separation noted in epidermolysis bullosa acquisita and herpes gestationis. Anaphylatoxin generation via the alternative pathway activation under ligth irradiation is implicated in the development of the immediate erythematous phototoxic reactions induced by such well-known chemicals as porphyrin, chlorthiazide, demethylchlortetracycline, and chlorpromazine. It is known that a direct exposure of the stratum corneum to living skin tissues induces intense infammatory changes. In vitro study demonstrated that the stratum corneum activates complement via the Antibody-independent alternative pathway to generate C5a anaphylatoxin. Thus, accumulated horny material from the follicular wall seems to play a crucial role in the induction of pustules in inflammatory acne lesions and abscesses in ruptured epidermal cysts via the activation of the alternative complement pathway. Meanwhile, in search for the chemotactic factors responsible for the transepidermal leukocyte chemotaxis noted in psoriasis and related sterile pustular dermatoses, we have detected the presence of unique chemotactic peptides in the scale extracts of lesional skin. Later studies identified the presence of C5a des Arg and IL-8 in this peptide fraction. The alternative complement pathway has been speculted for the complement activation at the subcorneal portion of the psoriatic epidermis by further immunological studies. Similar properties to activate the alternative complement pathway have been noted in various pathogenic fungi that induce inflammatory skin lesions. Generation of C5a anaphylatoxin beneath the fungus-laden stratum corneum seems to be responsible for the characteristic subcorneal pustule formation in superficial infections such as cutaneous candidiasis and dermatophytosis, whereas that around fungal spores in the dermis is presumed to play a role in the induction of mixed cell granuloma characterized by a dense neutrophil infiltration as noted in sporotrichosis and chromomycosis. Although Pityrosporum ovale constitutes ordinary skin microflora in seborrheic areas, its properties which activate complement via the alternative pathway are implicated in the pathogenesis of dandruff and seborrheic dermatitis, in which transepidermal neutrophil chemotaxis as noted in psoriasis is observed histopathologically.
Beno Michel - One of the best experts on this subject based on the ideXlab platform.
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Corticosteroids, aurothioglucose and soybean trypsin inhibitor do not prevent Pemphigus Antibody-induced acantholysis in vitro
British Journal of Dermatology, 2006Co-Authors: John R. Schiltz, Chung-hong Hu, Beno MichelAbstract:SUMMARY Hydrocortisone, triamcinolone acetonide, aurothioglucose and soybean trypsin inhibitor were added to normal human skin explants cultured with IgG from Pemphigus serum to determine if acantholysis could be prevented. At the therapeutic concentrations used none of these compounds prevented binding of the autoAntibody to the epidermal target cells, and none prevented acantholysis. These experiments support the concepts that the Pemphigus Antibody alone is responsible for producing the acantholytic lesions of Pemphigus, that the therapeutic effectiveness of steroids and gold salts is probably due to their ability to reduce serum autoAntibody titres and that Pemphigus acantholysis is probably not caused by a serine proteinase.
Luis A. Diaz - One of the best experts on this subject based on the ideXlab platform.
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Pemphigus Antibody induced phosphorylation of keratinocyte proteins.
Autoimmunity, 2006Co-Authors: David S. Rubenstein, Luis A. DiazAbstract:The Pemphigus family of autoimmune blistering diseases is characterized by an autoAntibody response to desmosomal cadherins in epithelia. Autoantibodies against desmogleins, desmosome cell adhesion molecules, induce loss of cell-cell adhesion that is characterized clinically by blister formation. The mechanism by which these autoantibodies induce loss of cell-cell adhesion is under active investigation, but appears to involve a coordinated intracellular response including activation of intracellular signaling and phosphorylation of a number of proteins in the target keratinocyte. Activation of p38 mitogen activated protein kinase may have a critical role in the acantholytic mechanism as inhibitors of p38MAPK block the ability of Pemphigus IgG to induce blistering in Pemphigus animal models.