Analysis of the T Cells that Are Potentially Involved in Autoantibody Production in Pemphigus Vulgaris

Hertl, Michael; Riechers, R.

doi:10.1111/j.1346-8138.1999.tb02086.x

Cited by 42 publications

(30 citation statements)

References 25 publications

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“…Healthy individuals who carry HLA class II alleles similar or identical to those highly prevalent in PV also develop autoreactive T-cell responses to Dsg 3. Autoreactive T-cells from PV patients produce both TH1 and TH2 cytokines, while autoreactive T-cells from healthy persons produce TH0 cytokines (Hertl and Riechers, 1999). Cytokines including interleukin-10 ( Toto et al, 2000), interleukin-6, interleukin-15, and tumor necrosis factor-alpha (Ameglio et al, 1999) are probably involved in PV .…”

Section: Cellular Immunity In Pvmentioning

confidence: 99%

“…CD28-deficient mice (lacking a co-stimulatory signal for T-lymphocyte activation) are much more sensitive to the development of PV than are wild-type mice . T-cell recognition of epitopes of Dsg 3 may be crucial for the initiation and perpetuation of the production of Dsg 3-specif- ic autoantibodies by B-lymphocytes (Hertl and Riechers, 1999). These autoreactive CD4+ T-cells preferentially produce TH2 cytokines such as interleukin 4 (IL-4), IL-6, and IL-10 (Wucherpfennig et al, 1995;Lin et al, 1997), but also TH1 cytokines such as gamma interferon (Hertl et al, 1998a,b;Hertl and Riechers, 1999).…”

Section: Cellular Immunity In Pvmentioning

confidence: 99%

“…T-cell recognition of epitopes of Dsg 3 may be crucial for the initiation and perpetuation of the production of Dsg 3-specif- ic autoantibodies by B-lymphocytes (Hertl and Riechers, 1999). These autoreactive CD4+ T-cells preferentially produce TH2 cytokines such as interleukin 4 (IL-4), IL-6, and IL-10 (Wucherpfennig et al, 1995;Lin et al, 1997), but also TH1 cytokines such as gamma interferon (Hertl et al, 1998a,b;Hertl and Riechers, 1999). Autoantibodies of the TH2-dependent IgG4 subtype are preferentially seen in active PV, while autoantibodies of the TH1-dependent IgG1 subclass predominate upon remission.…”

Section: Cellular Immunity In Pvmentioning

confidence: 99%

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Pemphigus Vulgaris: Update on Etiopathogenesis, Oral Manifestations, and Management

Scully

Challacombe

2002

Critical Reviews in Oral Biology & Medicine

139

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ABSTRACT:Pemphigus is a group of potentially life-threatening diseases characterized by cutaneous and mucosal blistering. There is a fairly strong genetic background to pemphigus with linkage to HLA class II alleles. Certain ethnic groups, such as Ashkenazi Jews and those of Mediterranean origin, are especially liable to pemphigus. Pemphigus vulgaris (PV), the most common and important variant, is an autoimmune blistering disease characterized by circulating pathogenic IgG antibodies against desmoglein 3 (Dsg3), about half the patients also having Dsg1 autoantibodies. Oral lesions are initially vesiculobullous but readily rupture, new bullae developing as the older ones rupture and ulcerate. Biopsy of perilesional tissue, with histological and immunostaining examinations, is essential to the diagnosis. Serum autoantibodies to either Dsg1 or Dsg3 are best detected by both normal human skin and monkey esophagus or by enzyme-linked immunosorbent assay (ELISA). Before the introduction of corticosteroids, pemphigus vulgaris was typically fatal mainly from dehydration or secondary systemic infections. Current treatment is largely based on systemic immunosuppression using systemic corticosteroids, with azathioprine, dapsone, methotrexate, cyclophosphamide, and gold as adjuvants or alternatives, but mycophenolate mofetil and intravenous immunoglobulins also appear promising.

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Section: Cellular Immunity In Pvmentioning

confidence: 99%

Section: Cellular Immunity In Pvmentioning

confidence: 99%

Section: Cellular Immunity In Pvmentioning

confidence: 99%

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Pemphigus Vulgaris: Update on Etiopathogenesis, Oral Manifestations, and Management

Scully

Challacombe

2002

Critical Reviews in Oral Biology & Medicine

139

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“…HLA-DRB1*04:02 is highly prevalent in PV, which provides the recognition of Dsg3 by CD4+ T cells. T cell-dependent B cell activation is critical for the induction of pathogenic IgG Abs [28][29][30][31].…”

Section: Introductionmentioning

confidence: 99%

Pemphigus: Subtypes, Clinical Features, Diagnosis, and Treatment

Kılıç¹

2018

Autoimmune Bullous Diseases

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Pemphigus is a group of autoimmune blistering disorders associated with autoantibodies against the keratinocyte cell surface. Pemphigus has three major variants: pemphigus vulgaris (PV), pemphigus foliaceus (PF), and paraneoplastic pemphigus (PNP) which all have further subtypes. The variants of pemphigus are classified depending upon the clinical and histological features, immunofluorescence staining pattern, and autoantibody profile of the disease. The onset and course of pemphigus appear on the basis of interaction between genetic predisposition and various triggering factors. Pemphigus vulgaris is the most commonly seen and representative clinical form of pemphigus. Together with clinical manifestations, the histopathological and immunopathological data support the diagnosis. As though some pemphigus variants, particularly pemphigus vulgaris and paraneoplastic pemphigus, have a mortality risk, early diagnosis is necessary and onset of treatment should be promptly initiated. In this chapter, firstly, classification of pemphigus is described. After then, clinical features, histopathological and immunopathological findings, target antigens, etiopathogenesis and comorbidities of each pemphigus variant are discussed briefly.Keywords: pemphigus, pemphigus variants, clinical manifestations, pathogenesis, histopathology, immunopathology IntroductionPemphigus is a distinct organ-specific autoimmune blistering disorder involving skin and mucous membranes associated with autoantibodies directed against desmosomes-intercellular adhesive molecule complex localized on the keratinocyte cell surface [1][2][3][4].© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Pemphigus has three major variants, which are classified depending on the basis of the clinical, histological features, immunofluorescence staining pattern and autoantibody profile of the disease including pemphigus vulgaris (PV), pemphigus foliaceus (PF), and paraneoplastic pemphigus (PNP), which all have further subtypes. Less frequently seen and newer variants of pemphigus include IgA pemphigus (IGAP) and pemphigus herpetiformis (PH) [1-6].The term "pemphigus" origins from the Greek word "pemphix", which has a meaning of "blister" [1]. It is a chronic potentially life-threating bullous disorder if not treated on time [4,7,8]. The phenotypes of pemphigus represent a complex spectrum with multiple genetic and environmental factors playing a role in disease pathogenesis [9,10].Together with clinical manifestations, the histopathological and immunopathological data support the diagnosis of the disease. The best site for the cutaneous biopsy for the appropriate histopathological examination is a fresh (< 24 h) small vesicle or 1/3 of the peripheral portion of the blister including the perilesional normal appearing s...

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“…Several diseases are defined by the production of antibodies and lymphocytes against infectious and environmental antigens. 6,7 Additionally, some may result from the triggering of an immune response against auto-antigens of the epidermis or dermis. 8 Today, any dermatologist opening a scientific journal on Immunology or Dermatology will observe that suppressor T cells, renamed regulatory T cellsTregs, have become a central concept in immunological vocabulary.…”

Section: Introductionmentioning

confidence: 99%

Papel das células T reguladoras no desenvolvimento de dermatoses

Lima

2006

An. Bras. Dermatol.

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T cells, particularly CD4+ T cells, have been associated with many aspects of skin disease. Current evidence suggests, however, that the role of CD4+ T lymphocytes in the development of cutaneous inflammation surpasses that of pro-inflammatory activation of effector T cells that direct the immune response. T cell subtypes with regulatory capacity, such as CD4+CD25+ high Tregs, have been identified. Recent observations suggest that in some skin diseases the function of these cells is modified. Therefore, the development and function of Treg cells in Dermatology are currently attractive topics because of their importance in controlling the immune system response against tumors and infectious diseases, as well as in inhibiting auto-immunity and allergy development. Therefore, defective regulatory mechanisms may allow a breach in peripheral immune tolerance followed by chronic inflammation and disease. Functional abnormalities and contributions of different subtypes of regulatory T cells in the development of dermatological illnesses are detailed in this review. Possible targets for therapy and modifications of regulatory T cells caused by immunomodulators used in Dermatology are highlighted. Keywords: Dermatology; Skin diseases; T-Lymphocytes; T-Lymphocytes, suppressor-inducer; Therapeutics Resumo: Células T, em particular as células T CD4+, têm sido associadas a muitos aspectos das doenças de pele. A evidência atual sugere, porém, que o papel dos linfócitos T CD4+ no desenvolvimento de inflamação cutânea excede o de ativador pró-inflamatório das células T de ação que dirigem a resposta imune. Subtipos de células T com capacidade reguladora, tais como

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Analysis of the T Cells that Are Potentially Involved in Autoantibody Production in Pemphigus Vulgaris

Cited by 42 publications

References 25 publications

Pemphigus Vulgaris: Update on Etiopathogenesis, Oral Manifestations, and Management

Pemphigus Vulgaris: Update on Etiopathogenesis, Oral Manifestations, and Management

Pemphigus: Subtypes, Clinical Features, Diagnosis, and Treatment

Papel das células T reguladoras no desenvolvimento de dermatoses

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