Acantholysis
Pemphigus
Desmoglein 3
Desmoglein 1
Desmosomes
A type of junction that attaches one cell to its neighbor. One of a number of differentiated regions which occur, for example, where the cytoplasmic membranes of adjacent epithelial cells are closely apposed. It consists of a circular region of each membrane together with associated intracellular microfilaments and an intercellular material which may include, for example, mucopolysaccharides. (From Glick, Glossary of Biochemistry and Molecular Biology, 1990; Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
Darier Disease
An autosomal dominantly inherited skin disorder characterized by warty malodorous papules that coalesce into plaques. It is caused by mutations in the ATP2A2 gene encoding SERCA2 protein, one of the SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES. The condition is similar, clinically and histologically, to BENIGN FAMILIAL PEMPHIGUS, another autosomal dominant skin disorder. Both diseases have defective calcium pumps (CALCIUM-TRANSPORTING ATPASES) and unstable desmosomal adhesion junctions (DESMOSOMES) between KERATINOCYTES.
Pemphigus, Benign Familial
An autosomal dominantly inherited skin disorder characterized by recurrent eruptions of vesicles and BULLAE mainly on the neck, axillae, and groin. Mutations in the ATP2C1 gene (encoding the secretory pathway Ca2++/Mn2++ ATPase 1 (SPCA1)) cause this disease. It is clinically and histologically similar to DARIER DISEASE - both have abnormal, unstable DESMOSOMES between KERATINOCYTES and defective CALCIUM-TRANSPORTING ATPASES. It is unrelated to PEMPHIGUS VULGARIS though it closely resembles that disease.
Keratinocytes
Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell.
Desmogleins
Autoantibodies
Immunoglobulin G
The anti-desmoglein 1 autoantibodies in pemphigus vulgaris sera are pathogenic. (1/42)
Pemphigus vulgaris and pemphigus foliaceus are two closely related, but clinically and histologically distinct, autoimmune skin diseases. The autoantigens for pemphigus vulgaris and pemphigus foliaceus are desmoglein 3 and desmoglein 1, respectively. The anti-desmoglein 1 antibodies in pemphigus foliaceus and anti-desmoglein 3 antibodies in pemphigus vulgaris are pathogenic as determined by immunoglobulin G passive transfer animal models. More than 50% of pemphigus vulgaris sera also contain anti-desmoglein 1 autoantibodies; however, the pathogenicity of the anti-desmoglein 1 autoantibodies in pemphigus vulgaris remains unknown. In this study, we used soluble recombinant extracellular domains of desmoglein 1 and desmoglein 3 to obtain affinity-purified anti-desmoglein 1 and anti-desmoglein 3 autoantibodies from pemphigus vulgaris sera and examined the pathogenicity of each fraction separately using the passive transfer mouse model. By immunoprecipitation, the purified anti-desmoglein 1 and anti-desmoglein 3 showed no cross-reactivity. The anti-desmoglein 1 autoantibodies in pemphigus vulgaris induced typical pemphigus foliaceus lesions in neonatal mice, whereas the anti-desmoglein 3 fraction induced pemphigus vulgaris-like lesions. In addition, the pathogenic anti-desmoglein 1 and anti-desmoglein 3 autoantibodies in pemphigus vulgaris had predominant IgG4 subclass specificity. These findings suggest that the anti-desmoglein 1 antibodies in pemphigus vulgaris are pathogenic. (+info)Immune modulation in pemphigus vulgaris: role of CD28 and IL-10. (2/42)
Pemphigus vulgaris (PV) is an autoimmune bullous skin disease characterized by Abs to the desmosomal cadherin desmoglein-3. Although the autoantibodies have been shown to be pathogenic, the role of the cellular immune system in the pathology of pemphigus-induced acantholysis is unclear. To further delineate the potential role of T cell-signaling pathways in the pathogenesis of PV, we performed passive transfer experiments with PV IgG in gene-targeted mutant mice. Our results demonstrated that CD28-deficient mice (lacking a costimulatory signal for T cell activation) are 5-fold more sensitive to the development of PV than wild-type mice. To evaluate whether the higher incidence of disease was due to an impairment in intercellular adhesion of keratinocytes, we performed an in vitro acantholysis, using CD28-/- mice keratinocytes. No alteration in in vitro adhesion was detected in CD28-/--type keratinocytes. Because the CD28 molecule plays a pivotal role in the induction of Th2 cytokines, we examined the levels of a prototypic Th2 cytokine (IL-10) in CD28-/- mice. Lower levels of IL-10 mRNA were found in lesions from CD28-/- mice. To determine whether pemphigus susceptibility in CD28-/- was related to IL-10 deficiency, we performed passive transfer experiments in IL-10-/- mice that demonstrated increased blisters compared with controls. To confirm that IL-10 is involved in the pathogenesis, rIL-10 was given with PV IgG. IL-10 significantly suppressed the disease activity. These data suggest a potential role of IL-10 in PV. (+info)In vitro and in vivo expression of interleukin-1alpha and tumor necrosis factor-alpha mRNA in pemphigus vulgaris: interleukin-1alpha and tumor necrosis factor-alpha are involved in acantholysis. (3/42)
Keratinocyte-derived cytokines have been implicated in the pathogenesis of a number of skin diseases. In this study we examined the possible role of keratinocyte-derived cytokines in the development of acantholysis in pemphigus vulgaris. Nineteen patients with pemphigus vulgaris, demonstrating the characteristic clinical, pathologic, and immunopathologic findings were studied. In situ immunolabeling demonstrated the presence of two cytokines interleukin-1alpha and tumor necrosis factor-alpha, in lesional and perilesional areas. Results were confirmed by reverse transcriptase-polymerase chain reaction, demonstrating overexpression of both cytokines in vivo. To study the role of these cytokines in the pathogenesis of pemphigus vulgaris both in vitro and in vivo studies were performed. The results of the in vitro study demonstrated that pemphigus vulgaris IgG induced interleukin-1alpha and tumor necrosis factor-alpha mRNA in the skin. The potential pathogenic role of these mediators was demonstrated by a blocking study using antibodies against human interleukin-1alpha and tumor necrosis factor-alpha in keratinocytes cultures. A combination of anti-interleukin-1alpha and anti-tumor necrosis factor-alpha antibodies inhibited in vitro pemphigus vulgaris IgG induced acantholysis. To confirm the role of interleukin-1 and tumor necrosis factor-alpha in pemphigus, we utilized passive transfer studies using interleukin-1 deficient mice (ICE-/-, interleukin-1beta-/-) and tumor necrosis factor-alpha receptor deficient mice (TNFR1R2-/-). Both groups demonstrated a decreased susceptibility to the passive transfer of pemphigus. Our data support the role of cytokines interleukin-1 and tumor necrosis factor-alpha in the pathogenesis of pemphigus vulgaris. (+info)Novel human alpha9 acetylcholine receptor regulating keratinocyte adhesion is targeted by Pemphigus vulgaris autoimmunity. (4/42)
Pemphigus vulgaris (PV) is a potentially fatal autoimmune mucocutaneous blistering disease. It was assumed that PV is caused by anti-desmoglein (Dsg) 3 autoimmunity because absorption of PV sera with a chimeric baculoprotein containing the Dsg 3 and IgG1 portions, rDsg3-Ig-His, eliminated disease-causing antibodies. In this study we demonstrate that rDsg3-Ig-His adsorbs out autoantibodies to different keratinocyte antigens, including a non-Dsg 3 130-kd polypeptide. Because the pool of disease-causing PV IgGs contains antibodies against the keratinocyte acetylcholine receptor (AChR), we sought to identify the targeted receptor(s). Preincubation of monkey esophagus with PV antibodies blocked specific staining of the keratinocyte cell membrane with rabbit monoepitopic antibody to alpha9 AChR, indicating that this first of its kind AChR with dual, muscarinic and nicotinic pharmacology is targeted by PV autoimmunity. Anti-alpha9 antibody stained keratinocytes in a fishnet-like intercellular pattern, and visualized a single band at approximately 50 kd in Western blots of keratinocyte membrane proteins. Using step-by-step reverse transcription polymerase chain reactions with primers based on known alpha9 sequence regions, we identified the complete reading frame of human alpha9. Its amino acid sequence showed 85% similarity with rat alpha9. Treatment of keratinocyte monolayers with anti-alpha9 antibody induced pemphigus-like acantholysis, which could be reversed either spontaneously or by using the cholinergic agonist carbachol. We conclude that alpha9 is coupled to physiological regulation of keratinocyte adhesion, and its interaction with PV IgG may lead to blister development. (+info)Antibodies against keratinocyte antigens other than desmogleins 1 and 3 can induce pemphigus vulgaris-like lesions. (5/42)
Pemphigus is an autoimmune disease of skin adhesion associated with autoantibodies against a number of keratinocyte antigens, such as the adhesion molecules desmoglein (Dsg) 1 and 3 and acetylcholine receptors. The notion that anti-Dsg antibodies alone are responsible for blisters in patients with pemphigus vulgaris (PV) stems from the ability of rDsg1 and rDsg3 to absorb antibodies that cause PV-like skin blisters in neonatal mice. Here, we demonstrate that PV IgGs eluted from rDsg1-Ig-His and rDsg3-Ig-His show similar antigenic profiles, including the 38-, 43-, 115-, and 190-kDa keratinocyte proteins and a non-Dsg 3 130-kDa polypeptide present in keratinocytes from Dsg 3 knockout mouse. We injected into Dsg 3-lacking mice the PV IgGs that did not cross-react with the 160-kDa Dsg 1 or its 45-kDa immunoreactive fragment and that showed no reactivity with recombinant Dsg 1. We used both the Dsg3(null) mice with a targeted mutation of the Dsg3 gene and the "balding" Dsg3(bal)/Dsg3(bal) mice that carry a spontaneous null mutation in Dsg3. These PV IgGs caused gross skin blisters with PV-like suprabasal acantholysis and stained perilesional epidermis in a fishnet-like pattern, indicating that the PV phenotype can be induced without anti-Dsg 3 antibody. The anti-Dsg 1 antibody also was not required, as its presence in PV IgG does not alter the PV-like phenotype in skin organ cultures and because pemphigus foliaceus IgGs produce a distinct phenotype in Dsg3(null) mice. Therefore, mucocutaneous lesions in PV patients could be caused by non-Dsg antibodies. (+info)Immunologic and histopathologic characterization of an active disease mouse model for pemphigus vulgaris. (6/42)
Pemphigus vulgaris is an autoimmune blistering disease of the skin and mucous membranes that is caused by anti-desmoglein 3 IgG autoantibodies. Recently, we generated an active disease mouse model for pemphigus vulgaris by adoptive transfer of splenocytes from immunized desmoglein 3-/- mice to Rag2-/- mice. In this study, we performed immunologic and histopathologic studies using this pemphigus vulgaris model in mice and compared the gross and microscopic phenotypes of pemphigus vulgaris model mice and desmoglein 3-/- mice. Pemphigus vulgaris model mice showed strong in vivo IgG, and weak IgA deposition on keratinocyte cell surfaces in stratified squamous epithelia, and produced circulating anti-desmoglein 3 IgG antibodies without apparent cross-reactivity to desmoglein 1, in enzyme-linked immunosorbent assays. The predominant IgG subclass was IgG1. Pemphigus vulgaris model mice and desmoglein 3-/- mice were almost indistinguishable in terms of both gross and microscopic findings. Both types of mice showed suprabasilar acantholysis in the stratified squamous epithelia, including the oral mucous membranes and traumatized skin around the snout or paws; however, some pemphigus vulgaris model mice demonstrated a more severe phenotype than desmoglein 3-/- mice. The esophagus and forestomach were affected in some pemphigus vulgaris model mice, but not in desmoglein 3-/- mice. Furthermore, eosinophilic spongiosis, which is found in early pemphigus vulgaris lesions in patients, was observed in pemphigus vulgaris model mice but not in desmoglein 3-/- mice. Pemphigus vulgaris model mice reflect several of the histopathologic and immunologic features seen in pemphigus vulgaris patients, and provide a valuable tool to investigate the pathophysiologic mechanisms of pemphigus vulgaris. (+info)Induction of pemphigus phenotype by a mouse monoclonal antibody against the amino-terminal adhesive interface of desmoglein 3. (7/42)
Pemphigus vulgaris (PV) is a life-threatening autoimmune blistering disease that is caused by IgG autoantibodies against the cadherin-type adhesion molecule desmoglein (Dsg)3. Previously, we have generated an active mouse model for PV by adoptive transfer of Dsg3(-/-) splenocytes. In this study, we isolated eight AK series, anti-Dsg3 IgG mAbs from the PV mouse model, and examined their pathogenic activities in induction of blister formation. Intraperitoneal inoculation of the AK23 hybridoma, but not the other AK hybridomas, induced the virtually identical phenotype to that of PV model mice or Dsg3(-/-) mice with typical histology of PV. Epitope mapping with domain-swapped and point-mutated Dsg1/Dsg3 molecules revealed that AK23 recognized a calcium-dependent conformational epitope on Dsg3, which consisted of the V3, K7, P8, and D59 Dsg3-specific residues that formed the adhesive interface between juxtaposed Dsg, as predicted by the crystal structure. The epitopes of the mAbs that failed to show apparent pathogenic activity were mapped in the middle to carboxyl-terminal extracellular region of Dsg3, where no direct intermolecular interaction was predicted. These findings demonstrate the pathogenic heterogeneity among anti-Dsg3 IgG Abs due to their epitopes, and suggest the direct inhibition of adhesive interaction of Dsg as an initial molecular event of blister formation in pemphigus. (+info)A case of focal acantholytic dyskeratosis occurring on both the lip and the anal canal. (8/42)
Focal acantholytic dyskeratosis has a distinctive histological pattern that is associated with various clinical expressions. It rarely occurs on the lip or the perianal area. We report a patient with focal acantholytic dyskeratosis occurring on both the upper lip and the anal canal. Histopathologically, the lesions showed hyperkeratosis, suprabasilar clefting, epidermal acantholysis and dyskeratosis. This case represents the first report of a focal acantholytic dyskeratosis occurring on both the lip and the anal canal. (+info)
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Seshadri, Divya (2013). "Acantholysis revisited: Back to basics". Indian J Dermatol Venereol Leprol. 79 (1): 120-6. doi:10.4103 ...
Cantharidin
The process leads to the loss of cellular connections (acantholysis) and ultimately blistering of the skin. Lesions heal ... Bertaux, B.; Prost, C.; Heslan, M.; Dubertret, L. (1988). "Cantharide acantholysis: endogenous protease activation leading to ...
Pemphigus foliaceus
This in turn causes a loss of adhesion with acantholysis as a result. The National Institute of Arthritis and Musculoskeletal ...
Hailey-Hailey disease
In addition to blistering, other symptoms which accompany HHD include acantholysis, erythema and hyperkeratosis. The cause of ... causing acantholysis, blisters and rashes. There is no known cure.[citation needed] While the term pemphigus typically refers ...
Pemphigus
The pathologist looks for an intraepidermal vesicle caused by the breaking apart of epidermal cells (acantholysis). Thus, the ... a phenomenon called acantholysis. This causes blisters that slough off and turn into sores. In some cases, these blisters can ... and acantholysis. The least common and most severe type of pemphigus is paraneoplastic pemphigus (PNP). This disorder is a ... acantholysis), and by the presence of pathogenic (predominantly IgG) autoantibodies reacting against epithelial adhesion ...
IgA pemphigus
... and acantholysis.: 465 Early descriptions were made by Darrell Wilkinson, a British dermatologist. Pemphigus List of cutaneous ...
Desmosome
PV is manifested by suprabasal acantholysis, or blisters in the mucous membrane and blisters in the epidermis. PF patients have ...
Pemphigus vulgaris
These blisters are due to acantholysis, or breaking apart of intercellular connections through an autoantibody-mediated ...
Blister beetle dermatitis
This results from the disruption of tonofilaments in the desmosomes with acantholysis and intra-epidermal blister formation. " ...
Transient acantholytic dermatosis
Grover's disease (GD) is a polymorphic, pruritic, papulovesicular dermatosis characterized histologically by acantholysis: 529 ...
Desmoglein-3
... are present in sera from patients with paraneoplastic pemphigus and cause acantholysis in vivo in neonatal mice". The Journal ...
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... is characterized by a tubular microscopic pattern and keratinocyte acantholysis. Basaloid squamous cell carcinoma is ...
Pemphigoid
... pemphigoid does not feature acantholysis, a loss of connections between skin cells. Pemphigoid is more common than pemphigus, ...
Galli-Galli disease
... nondyskeratotic acantholysis. List of cutaneous conditions Skin lesion James, William; Berger, Timothy; Elston, Dirk Andrews' ...
Paraneoplastic pemphigus
... epidermal acantholysis (breaking apart of the skin), dyskeratotic keratinocytes and vacuolar changes in the layers of the skin ... Histologic evidence of acantholysis (loss of intercellular connections leading to breaking apart of the skin; lesion) Direct ...
Skin condition
Poikiloderma Hyperkeratosis Parakeratosis Hypergranulosis Acanthosis Papillomatosis Dyskeratosis Acantholysis Spongiosis ...
List of MeSH codes (C17)
... acantholysis MeSH C17.800.865.187 - blister MeSH C17.800.865.360 - dermatitis herpetiformis MeSH C17.800.865.385 - eczema, ...
Acantholysis
... is the loss of intercellular connections, such as desmosomes, resulting in loss of cohesion between keratinocytes ... ISBN 0-7216-0187-1. "Acantholysis - Medical Definition from MediLexicon". medilexicon.com. Archived from the original on 2016- ...
Acantholysis - Wikipedia
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Several hypotheses for the mechanisms of acantholysis induction by PV-IgG exist, but the actual mechanism is not clear as yet. ... Several hypotheses for the mechanisms of acantholysis induction by PV-IgG exist, but the actual mechanism is not clear as yet. ... Several hypotheses for the mechanisms of acantholysis induction by PV-IgG exist, but the actual mechanism is not clear as yet. ... Several hypotheses for the mechanisms of acantholysis induction by PV-IgG exist, but the actual mechanism is not clear as yet. ...
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Acantholysis has been reported as an additional histologic finding in pityriasis rubra pilaris. [9] Acantholysis may be ... Howe K, Foresman P, Griffin T, Johnson W. Pityriasis rubra pilaris with acantholysis. J Cutan Pathol. 1996 Jun. 23(3):270-4. [ ... The presence of acantholysis, hypergranulosis, follicular plugging, and the absence of dilated capillaries and epidermal ... Avitan-Hersh E, Bergman R. The Incidence of Acantholysis in Pityriasis Rubra Pilaris-Histopathological Study Using Multiple- ...
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Acantholysis: loss of appropriate keratinocyte cell-cell contact (pemphigus, transient acantholytic dermatosis, Hailey-Hailey, ... Presence or absence of acantholysis * Characterization of any associated inflammatory infiltrate * Immunofluorescent pattern * ... Large intraepidermal bullae without acantholysis may represent healed subepidermal bullae (re-epitheliazation phenomemon) * ...
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Follicular acantholysis may also be a subtle histologic manifestation of PV, as reported by Mahalingam. [4] This observation of ... Mahalingam M. Follicular acantholysis: a subtle clue to the early diagnosis of pemphigus vulgaris. Am J Dermatopathol 2005;27: ... 3] The presence of Dsg3 in the hair follicle epithelium would explain the presence of acantholysis in the adnexal epithelium in ... The biopsy specimen from all these cases showed typical microscopic features of PV, such as suprabasal bulla, acantholysis and ...
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Figure 3:: Acantholysis and dyskeratosis with the presence of corps ronds and grains (H and E, ×400) ... Figure 2:: Acantholysis throughout the epidermis, hyperkeratosis, and parakeratosis were found in the epidermis with chronic ... The histologic features of papular acantholytic dyskeratosis are acantholysis which may involve the full thickness of the ... The histopathologic findings showed acantholysis throughout the epidermis with dyskeratotic cells resembling corps ronds and ...
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Keratinocytes9
- Acantholysis is the loss of intercellular connections, such as desmosomes, resulting in loss of cohesion between keratinocytes, seen in diseases such as pemphigus vulgaris. (wikipedia.org)
- Endemic pemphigus foliaceus (PF), also known as fogo selvagem, is a skin autoimmune blistering disease due to acantholysis, the loss of adhesion among keratinocytes. (bartleby.com)
- The biopsy demonstrates suprabasilar acantholysis, which means that there is a split within the epidermis above the basal keratinocytes. (clinicaladvisor.com)
- In this condition there is prominent atypia of the keratinocytes , with acantholysis frequently present through all layers of the involved epidermis. (dermnetnz.org)
- Their impaired biological function leads to loss of adhesion, acantholysis and apoptosis of keratinocytes. (altmeyers.org)
- Pemphigus vulgaris (PV) is an autoimmune bullous disease caused by acantholysis of keratinocytes due to pathogenic desmoglein-3 autoantibodies. (biomedcentral.com)
- Autoantibodies against the desmosomal component desmoglein-3 are implicated in acantholysis of keratinocytes, leading to formation of clefts or bullae [ 1 ]. (biomedcentral.com)
- The molecular background of the blistering is the interference of the adhesion between the keratinocytes (acantholysis) by the autoantibodies against intercellular adhesion structures. (svarlifescience.com)
- Due to the decrease in the active SERCA2 protein, the affected keratinocytes cannot conduct normal Ca metabolism and result in the individual dyskeratosis and acantholysis. (nii.ac.jp)
Epidermal9
- The term 'epidermal necrolysis' (EN) is used in this article to describe the spectrum of disease that includes SJS and TEN. (medscape.com)
- [ 1 ] They are simply described together as epidermal necrolysis (EN). (medscape.com)
- Circulating autoantibodies bind to epidermal cell membrane and cause cell-cell detachment (acantholysis), leading to epidermal tissue damage and cell death. (tau.ac.il)
- We have previously reported on apoptosis induction in PV-IgG-mediated epidermal tissue and cell damage as a possible mechanism of acantholysis and cell death (Wang et al. (tau.ac.il)
- The presence of acantholysis, hypergranulosis, follicular plugging, and the absence of dilated capillaries and epidermal pustulation may help distinguish pityriasis rubra pilaris from psoriasis. (medscape.com)
- Lesions resembling pemphigus foliaceus reveal superficial epidermal acantholysis, while those resembling pemphigus vulgaris reveal suprabasal acantholysis. (medscape.com)
- Loss of epidermal cohesion in normal skin explants incubated with pemphigus foliaceous IgG was dependent upon the addition of plasminogen and was inhibited by aprotinin or lima bean trypsin inhibitor, which indicated that plasmin is the active enzyme in producing acantholysis. (cdc.gov)
- Intraepidermal vesicle produced by profound degeneration of epidermal cells, resulting in marked acantholysis. (dermpathdiagnostics.com)
- Both models demonstrated a similar timecourse of sunburn cell (SBC) formation, epidermal necrosis, acantholysis and parakeratosis, and regeneration. (mattek.com)
Focal acantholysis2
- This condition is histologically variable, and the key finding on pathology is focal acantholysis. (logicalimages.com)
- Warty dyskeratoma (WD) is an uncommon skin tumor that histologically presents as focal acantholysis and dyskeratosis and is a common finding among acantholytic diseases such as Darier's disease. (bvsalud.org)
Subcorneal3
- Histologically, subcorneal acantholysis and bulla formation are seen. (pathos223.com)
- Would show subcorneal pustules with neutrophils and acantholysis. (partishpresademokrate.com)
- b) Histology of the skin shows subcorneal acantholysis and blister filled with neutrophils. (medicalkidnap.com)
Histopathology2
- Histopathology reveals acantholysis with varying degrees of dyskeratosis, and direct and indirect immunofluorescence are negative in almost all cases studied. (actasdermo.org)
- Histopathology confirms acantholysis, and keeping pores and noninflammatory and why we caution in dosage forms. (gors.nl)
Histologically1
- Group of chronic blistering diseases characterized histologically by ACANTHOLYSIS and blister formation within the EPIDERMIS. (lookformedical.com)
Bullae1
- It is characterized by intraepidermal bullae with neutrophils, some acantholysis and eosinophils. (alwaysayurveda.net)
Apoptosis1
- The acantholytic effect caused by PV-IgG binding to cell surface receptors begins with and depends on cell surface receptor (EGFR) activation of intracellular signaling pathways (ERK pathway) and apoptosis induction (FasR pathway), which later lead to major cell-cell separation (acantholysis) and cell death. (tau.ac.il)
Separation1
- c) completion angiogram after removal of the pinna (fig. Streptococcus pneumoniae and the incision and surrounding skindemonstrate acantholysis (separation of the bone and the, in newborns. (berea.edu)
Matching direct immunofluorescence1
- In this related condition intraepidermal acantholysis is seen within the lower suprabasal epidermis, with matching direct immunofluorescence at this level. (dermnetnz.org)
Involvement1
- The specific tyrosine kinase inhibitor AG1478 abrogated EGFR autophosphorylation, cell death, FasL appearance and acantholysis, all induced by PV-IgG, in parallel, confirming the involvement of EGFR in this Fas apoptotic cascade. (tau.ac.il)
Disease2
- In addition to pigmentation changes, individuals with Galli-Galli disease also have a breakdown of cells in the outer layer of skin (acantholysis). (medlineplus.gov)
- Background: Pemphigus vulgaris (PV) is an autoimmune disease characterized by acantholysis. (bezmialem.edu.tr)
Lymphocytes1
- Le pourcentage de CD44 dans les lymphocytes T périphériques était significativement plus élevé chez les patients que chez les témoins, comme détecté par la cytométrie en flux. (who.int)
Mechanism3
- It was previously believed that widespread keratinocyte death in EN is predominantly mediated by soluble Fas-ligand and that intravenous immunoglobulin therapy is useful in blocking this mechanism with resultant survival benefits. (medscape.com)
- Several hypotheses for the mechanisms of acantholysis induction by PV-IgG exist, but the actual mechanism is not clear as yet. (tau.ac.il)
- The mechanism by which mutant ATPC1 causes acantholysis is unknown, but it may be through abnormally elevated cytoplasmic calcium or abnormally low Golgi Ca(2+) levels. (haileyhailey.com)
Skin1
- Acantholysis can cause skin irritation and itchiness and lead to reddened or missing patches of skin (erosions). (medlineplus.gov)
Role2
Superficial3
- Superficial pustular dermatosis with acantholysis in a Limousin calf. (bsvp.org)
- A diagnosis of Superficial pustular dermatosis with acantholysis was made. (bsvp.org)
- A punch biopsy of the right abdomen was performed and revealed psoriasiform epidermal hyperplasia, focal parakeratosis, and acantholysis throughout the superficial spinous and granular layers (Figure 3). (skinofcolorupdate.com)
Congenital2
- A congenital defect leading to acantholysis seems probable in this calf, though the expression appears milder than in the inherited conditions described. (bsvp.org)
- DSP missense variant in a Scottish Highland calf with congenital ichthyosis, alopecia, acantholysis of the tongue and corneal defects. (unibe.ch)
Epidermis1
- The epidermis showed mild and diffuse spongiosis with focal exocytosis of neutrophils without acantholysis. (cdlib.org)
Spongiosis1
- Sometimes it showed spongiosis, but the acantholysis was frequently very prominent. (bsvp.org)
Intercellular1
- Typical epithelial lesions include hyperkeratosis (increased thickness of the keratin layer), acanthosis (increased thickness of the prickle cell layer with or without associated hyperkeratosis), atrophy (thinning of the epithelium, often associated with incomplete keratinization), or acantholysis (loss of the intercellular attachments in the prickle cell layer leading to separation of the cells). (antimicrobe.org)
Immunofluorescence1
- The key to diagnosing SPD is a biopsy demonstrating a sterile subcorneal pustule filled with neutrophils, absence of acantholysis, and negative immunofluorescence. (cdlib.org)
Pemphigus3
- Acantholysis is a feature of some autoimmune disease processes such as pemphigus foliaceus but in an individual of this age, an autoimmune process was unlikely. (bsvp.org)
- Histologic assessment of the lesion identified acanthosis and acantholysis with dermal eosinophils consistent with pemphigus vegetans. (jofskin.org)
- PEMPHIGUS vulgaris is a severe and often fatal blistering disease, affecting the skin and mucous membranes, in which intraepithelial vesicles form as a result of a distinctive process of cell detachment termed acantholysis. (elsevier.com)
Epithelial1
- Inherited disease characterised by acantholysis due to defective epithelial adhesion is also described in humans and dogs. (bsvp.org)
Histologic2
- The histologic picture in dogs and in the Angus calves would appear to show a more extensive pattern of acantholysis than is present in this individual. (bsvp.org)
- b) Histologic findings that reflect the variability of the cutaneous lesions, showing acantholysis, lichenoid, or interface change. (mhmedical.com)