The final destiny of acantholytic cells in pemphigus is Fas mediated

被引:20
作者
Pacheco-Tovar, M. G. [1 ]
Avalos-Diaz, E. [1 ]
Vega-Memije, E. [2 ]
Bollain-y-Goytia, J. J. [1 ]
Lopez-Robles, E. [1 ]
Hojyo-Tomoka, M. T. [2 ]
Dominguez-Soto, L. [2 ]
Herrera-Esparza, R. [1 ]
机构
[1] Univ Autonoma Zacatecas, Dept Immunol, Unidad Acad Biol Expt, Guadalupe, Zacatecas, Mexico
[2] Hosp Manuel Gea Gonzalez, Dept Dermatol, Mexico City, DF, Mexico
关键词
Acantholysis; apoptosis; Fas; CD8; cells; pemphigus; T-LYMPHOCYTES; ANTIBODIES; MECHANISMS; DESMOGLEIN; EXPRESSION; APOPTOSIS; LIGAND; IGG;
D O I
10.1111/j.1468-3083.2009.03162.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Pemphigus is an autoimmune disease characterized by the formation of intra-epidermal blisters. Patients develop auto-antibodies against desmoglein 1 and 3 proteins and induce acantholysis. This work addresses the issue of whether the Fas pathway mediates acantholysis. Furthermore, the possible suppliers of the Fas pathway were investigated. Seventeen biopsies of pemphigus patients were studied by haematoxylin and eosin staining, and apoptosis was defined by TUNEL. The expression of Fas, FasL and caspase 3 was studied by in situ hybridization and immunohistochemistry. Cell infiltrates were studied by immunofluorescence with monoclonal anti-CD3, CD4, CD8, CD19 and CD69. All of the biopsies showed intra-epidermal blisters, acantholytic cells and inflammatory infiltrates. The blisters expressed Fas, FasL and caspase 3. Cell infiltrates were composed of CD8 and a few CD4(+)CD69(+) cells. Additionally, CD19(+) cells were detected. Interestingly, the Fas expression was increased in acantholytic cells and perilesional keratinocytes. Incidentally, these cells exhibited apoptotic features. Interestingly, the CD8 cells expressed FasL. This paper presents the morphological evidence that apoptosis and acantholysis are linked. Therefore, the Fas pathway is associated with CD8 cells in pemphigus lesions. None declared.
引用
收藏
页码:697 / 701
页数:5
相关论文
共 20 条
[11]   Mechanisms of acantholysis in Pemphigus foliaceus [J].
Espana, A ;
Diaz, LA ;
Mascaro, JM ;
Giudice, GJ ;
Fairley, JA ;
Till, GO ;
Liu, Z .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1997, 85 (01) :83-89
[12]   AUTOREACTIVE CYTO-TOXIC LYMPHOCYTES-T IN PEMPHIGUS AND PEMPHIGOID [J].
GRANDO, SA ;
GLUKHENKY, BT ;
DRANNIK, GN ;
KOSTROMIN, AP ;
BOIKO, YY ;
SENYUK, OF .
AUTOIMMUNITY, 1989, 3 (04) :247-260
[13]   Perforin, granzyme B, and FasL expression by peripheral blood T lymphocytes in emphysema [J].
Morissette, Mathieu C. ;
Parent, Julie ;
Milot, Julie .
RESPIRATORY RESEARCH, 2007, 8 (1)
[14]   Humanization and epitope mapping of neutralizing anti-human fas ligand monoclonal antibodies: Structural insights into Fas/Fas ligand interaction [J].
Nisihara, T ;
Ushio, Y ;
Higuchi, H ;
Kayagaki, N ;
Yamaguchi, N ;
Soejima, K ;
Matsuo, S ;
Maeda, H ;
Eda, Y ;
Okumura, K ;
Yagita, H .
JOURNAL OF IMMUNOLOGY, 2001, 167 (06) :3266-3275
[15]   Pemphigus vulgaris autoantibodies induce apoptosis in HaCaT keratinocytes [J].
Pelacho, B ;
Natal, C ;
España, A ;
Sánchez-Carpintero, I ;
Iraburu, MJ ;
López-Zabalza, MJ .
FEBS LETTERS, 2004, 566 (1-3) :6-10
[16]   The molecular basis for apoptotic defects in patients with CD95 (Fas/Apo-1) mutations [J].
Vaishnaw, AK ;
Orlinick, JR ;
Chu, JL ;
Krammer, PH ;
Chao, MV ;
Elkon, KB .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 103 (03) :355-363
[17]   Possible apoptotic mechanism in epidermal cell acantholysis induced by pemphigus vulgaris autoimmunoglobulins [J].
Wang, X ;
Brégégère, F ;
Frusic-Zlotkin, M ;
Feinmesser, M ;
Michel, B ;
Milner, Y .
APOPTOSIS, 2004, 9 (02) :131-143
[18]   Pemphigus foliaceus IgG causes dissociation of desmoglein 1-containing junctions without blocking desmoglein 1 transinteraction [J].
Waschke, J ;
Bruggeman, P ;
Baumgartner, W ;
Zillikens, D ;
Drenckhahn, D .
JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (11) :3157-3165
[19]   CD8+ T cells promote inflammation and apoptosis in the liver after sepsis -: Role of Fas-FasL [J].
Wesche-Soldato, Doreen E. ;
Chung, Chun-Shiang ;
Gregory, Stephen H. ;
Salazar-Mather, Thais P. ;
Ayala, Carol A. ;
Ayala, Alfred .
AMERICAN JOURNAL OF PATHOLOGY, 2007, 171 (01) :87-96
[20]   The pathophysiology of autoimmune blistering diseases [J].
Yancey, KB .
JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (04) :825-828