Acantholysis: Separation of the prickle cells of the stratum spinosum of the epidermis, resulting in atrophy of the prickle cell layer. It is seen in diseases such as pemphigus vulgaris (see PEMPHIGUS) and DARIER DISEASE.Pemphigus: Group of chronic blistering diseases characterized histologically by ACANTHOLYSIS and blister formation within the EPIDERMIS.Desmoglein 3: A desmosomal cadherin that is an autoantigen in the acquired skin disorder PEMPHIGUS VULGARIS.Desmoglein 1: A desmosomal cadherin that is an autoantigen in the acquired skin disorder PEMPHIGUS FOLIACEUS.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.Blister: Visible accumulations of fluid within or beneath the epidermis.Desmogleins: A group of desmosomal cadherins with cytoplasmic tails that resemble those of classical CADHERINS.Autoantibodies: Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.Immunoglobulin G: The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.Skin: The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
(1/42) The anti-desmoglein 1 autoantibodies in pemphigus vulgaris sera are pathogenic.

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)

(2/42) Immune modulation in pemphigus vulgaris: role of CD28 and IL-10.

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)

(3/42) 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.

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)

(4/42) Novel human alpha9 acetylcholine receptor regulating keratinocyte adhesion is targeted by Pemphigus vulgaris autoimmunity.

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)

(5/42) Antibodies against keratinocyte antigens other than desmogleins 1 and 3 can induce pemphigus vulgaris-like lesions.

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)

(6/42) Immunologic and histopathologic characterization of an active disease mouse model for pemphigus vulgaris.

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)

(7/42) Induction of pemphigus phenotype by a mouse monoclonal antibody against the amino-terminal adhesive interface of desmoglein 3.

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)

(8/42) A case of focal acantholytic dyskeratosis occurring on both the lip and the anal canal.

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)

*  Transient acantholytic dermatosis
Grover's disease (GD) is a polymorphic, pruritic, papulovesicular dermatosis characterized histologically by acantholysis with ...
*  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. Retrieved 2017-04-22. ...
*  Pemphigus foliaceus
This in turn causes a loss of adhesion with acantholysis as a result. The National Institute of Arthritis and Musculoskeletal ...
*  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. 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 mucus membrane and blisters in the epidermis. PF patients have ...
*  Blister beetle dermatitis
This results from the disruption of tonofilaments in the desmosomes with acantholysis and intra-epidermal blister formation. " ...
*  Squamous cell carcinoma
... characterized by a tubular microscopic pattern and keratinocyte acantholysis. Basaloid squamous cell carcinoma is characterized ...
*  Desmoglein-3
... are present in sera from patients with paraneoplastic pemphigus and cause acantholysis in vivo in neonatal mice". J. Clin. ...
*  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 James, William; Berger, Timothy; Elston, Dirk Andrews' Diseases of ...
*  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 ...
*  Hailey-Hailey disease
... causing acantholysis, blisters and rashes. There is no known cure. The differential diagnosis includes intertrigo, candidiasis ...
*  Cutaneous condition
Hyperkeratosis Parakeratosis Hypergranulosis Acanthosis Papillomatosis Dyskeratosis Acantholysis Spongiosis Hydropic swelling ...
*  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 ...
Definition of ACANTHOLYSIS (Meaning of ACANTHOLYSIS), a 12 Letter Word  Definition of ACANTHOLYSIS (Meaning of ACANTHOLYSIS), a 12 Letter Word
... and antonyms of the term ACANTHOLYSIS in the Online Dictionary. What is a 12 letter word that starts with A? ... ACANTHOLYSIS: Review the definition, meaning, pronunciation, explanation, synonyms, ...
more infohttp://www.hyperdictionary.com/dictionary/acantholysis
Activity of the hSPCA1 Golgi Ca2+ pump is essential for Ca2+-mediated Ca2+ response and cell viability in Darier disease |...  Activity of the hSPCA1 Golgi Ca2+ pump is essential for Ca2+-mediated Ca2+ response and cell viability in Darier disease |...
hSPCA1 deficiency causes acantholysis, whereas mutations in the gene encoding SERCA2 cause both acantholysis and apoptosis. In ... turn, the clinical phenotype of acantholysis plus apoptosis in DD probably reflects the varied functions of the keratinocyte ...
more infohttp://jcs.biologists.org/content/119/4/671
Targeted disruption of the pemphigus vulgaris antigen (desmoglein 3)  by P J. Koch, M G. Mahoney et al.  Targeted disruption of the pemphigus vulgaris antigen (desmoglein 3) " by P J. Koch, M G. Mahoney et al.
Traumatized skin also had crusting and suprabasilar acantholysis. Runted mice showed hair loss at weaning. The runting and hair ... Indeed, oropharyngeal biopsies showed erosions with histology typical of PV, including suprabasilar acantholysis and ... Traumatized skin also had crusting and suprabasilar acantholysis. Runted mice showed hair loss at weaning. The runting and hair ... Indeed, oropharyngeal biopsies showed erosions with histology typical of PV, including suprabasilar acantholysis and ...
more infohttps://mouseion.jax.org/stfb1990_1999/991/
IJMS  | Free Full-Text | Overlapping ATP2C1 and ASTE1 Genes in Human Genome: Implications for SPCA1 Expression? | HTML  IJMS | Free Full-Text | Overlapping ATP2C1 and ASTE1 Genes in Human Genome: Implications for SPCA1 Expression? | HTML
... characterized by acantholysis (a disruption of cell-cell contacts) in the suprabasal layers of the skin [6]. SPCA1 protein ...
more infohttp://www.mdpi.com/1422-0067/14/1/674/htm
Dariers disease | Skin Support  Darier's disease | Skin Support
It is a rare inherited skin condition characterised by the loss of binding (acantholysis) between skin surface cells and there ...
more infohttp://skinsupport.org.uk/conditions-details/dariers-disease
Acantholysis - Wikipedia  Acantholysis - Wikipedia
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. Retrieved 2017-04-22. ...
more infohttps://en.wikipedia.org/wiki/Acantholysis
Acantholysis - definition of acantholysis by The Free Dictionary  Acantholysis - definition of acantholysis by The Free Dictionary
acantholysis synonyms, acantholysis pronunciation, acantholysis translation, English dictionary definition of acantholysis. ... Noun 1. acantholysis - a breakdown of a cell layer in the epidermis disease of the skin, skin disease, skin disorder - a ... acantholysis. Also found in: Thesaurus, Medical, Wikipedia.. Related to acantholysis: pemphigus, acanthosis, dyskeratosis, ... Acantholysis - definition of acantholysis by The Free Dictionary https://www.thefreedictionary.com/acantholysis ...
more infohttps://www.thefreedictionary.com/acantholysis
Acantholysis | definition of acantholysis by Medical dictionary  Acantholysis | definition of acantholysis by Medical dictionary
... acantholysis explanation free. What is acantholysis? Meaning of acantholysis medical term. What does acantholysis mean? ... Looking for online definition of acantholysis in the Medical Dictionary? ... acantholysis. Also found in: Dictionary, Thesaurus, Wikipedia.. Related to acantholysis: pemphigus, acanthosis, dyskeratosis, ... acantholysis. Splitting apart of layers of cells in the epidermis often top form a blister.. acantholysis. atrophy or ...
more infohttp://medical-dictionary.thefreedictionary.com/acantholysis
Incidental Cutaneous Reaction Patterns: Epidermolytic Hyperkeratosis, Acantholytic Dyskeratosis, and Hailey-Hailey-Like...  Incidental Cutaneous Reaction Patterns: Epidermolytic Hyperkeratosis, Acantholytic Dyskeratosis, and Hailey-Hailey-Like...
E. Sanchez Yus, L. Requena, P. Simon, and C. Martin de Hijas, "Incidental acantholysis," Journal of Cutaneous Pathology, vol. ... Figure 4: Incidental focus of Hailey-Hailey-like acantholysis, occurring in association with a benign keratosis with features ... In the largest studies, incidental acantholysis was identified in 14 of 9000 specimens [35], and incidental FAD was identified ... Occasionally, these patterns are combined in a single specimen, and foci of acantholysis with overlapping histologic patterns ...
more infohttps://www.hindawi.com/journals/jsc/2011/645743/
Transitory acantholysis dermatous Grovera.  Transitory acantholysis dermatous Grovera.
... Dermatit Grovera presence is original reaction of skin by astenised people, ...
more infohttps://doclecture.net/1-146.html
Browse In Dentistry,  Overview Page | Oxford Reference  Browse In Dentistry, Overview Page | Oxford Reference
acantholysis Reference type: Overview Page. Subject: Medicine and health, Dentistry. The breakdown of epidermal or epithelial ...
more infohttps://www.oxfordreference.com/browse?btog=chap&pageSize=20&sort=titlesort&t=ORO%3AMED00400&type_0=overviewpages
ultrastructure  ultrastructure
Acantholysis was present in two of five N+ biopsies, but only in the upper epidermal layers. The lesional skin biopsies ... Conclusion We propose the following mechanism for acantholysis in PF: initially PF IgG causes a depletion of non-junctional ... Objectives To examine early acantholysis in skin of PF patients at an ultrastructural level. ... ongoing depletion of Dsg1 will finally result in a total disappearance of desmosomes and subsequent acantholysis. ...
more infohttp://www.pemphigus.org/tag/ultrastructure/
Around the Globe | International Pemphigus Pemphigoid Foundation (IPPF) - Part 8  Around the Globe | International Pemphigus Pemphigoid Foundation (IPPF) - Part 8
Acantholysis was present in two of five N+ biopsies, but only in the upper epidermal layers. The lesional skin biopsies ... Conclusion We propose the following mechanism for acantholysis in PF: initially PF IgG causes a depletion of non-junctional ... Objectives To examine early acantholysis in skin of PF patients at an ultrastructural level. ... is an autoimmune blistering skin disorder characterized by the presence of suprabasal acantholysis and autoantibodies against ...
more infohttp://www.pemphigus.org/category/around-the-globe/page/8/
Subcorneal Pustular Dermatosis: Overview of Subcorneal Pustular Dermatosis, Pathophysiology of Subcorneal Pustular Dermatosis,...  Subcorneal Pustular Dermatosis: Overview of Subcorneal Pustular Dermatosis, Pathophysiology of Subcorneal Pustular Dermatosis,...
Acantholysis is not prominent; however, it has been reported in older lesions. See the image below. ... Unlike pemphigus, a predominance of neutrophils and an absence or moderate acantholysis is observed; additionally, the ...
more infohttps://emedicine.medscape.com/article/1124252-overview
Paraneoplastic Pemphigus - Trip Database  Paraneoplastic Pemphigus - Trip Database
Paraneoplastic pemphigus acantholysis. . . . Investigations Serum electrolytes, glucose and bicarbonate are essential to assess ...
more infohttps://www.tripdatabase.com/search?criteria=Paraneoplastic+Pemphigus&page=8
  • Other proposed mechanisms for biochemical acantholysis include activation of proteolytic enzymes and production of plasmin. (statpearls.com)
  • Although detailed mechanisms of acantholysis of these blistering diseases have not been fully clarified, abnormal expression of cadherins caused by altered Ca2+ concentration due to the binding of autoantibodies to cell surface or by mutations in Ca2+ pumps is suggested to be involved in mechanisms of acantholysis of these autoimmune and inherited blistering diseases. (haileyhailey.com)