Further support for a role for Th2-like cytokines in blister formation of pemphigus.
Pemphigus vulgaris and pemphigus foliaceus are commonly known as antibody-mediated bullous diseases. However, recently a role for infiltrating cells as contributors to the pathogenesis of these diseases has been suggested. The aims of our study were to characterize the immunophenotype of the cellular infiltrate of pemphigus lesional skin and to study the cytokines secreted. We have therefore performed an immunohistochemical study with a large panel of monoclonal antibodies (to CD3, CD4, CD8, CD25, CD30, myeloperoxidase, eosinophil cationic protein EG2, tryptase, human interleukin (IL)-2, human IL-4, human IL-5, human IL-6, human IL-8, and interferon (IFN)-gamma using the alkaline phosphatase-antialkaline phosphatase procedure on lesional and uninvolved skin of six patients with clinical, histological, and immunofluorescent proven pemphigus. We also performed RT-PCR in order to demonstrate mRNA expression of the cytokines of interest. Our results suggest the presence of a T cell population with a prevalent Th2-like cytokine pattern in lesional skin. In addition, we demonstrate a consistent number of granulocytes and mast cells that show clear signs of activation. These data suggest the involvement of an inflammatory infiltrate in the production of pemphigus lesions. In particular, we assume that Th2 cells may be implicated in the very early stages of autoimmune response, concluding that they exert broad activity in blister formation.
Caproni
M
M
Department of Dermatological Sciences, University of Florence, Florence, Italy.
Giomi
B
B
Cardinali
C
C
Salvatore
E
E
Pestelli
E
E
D'Agata
A
A
Bianchi
B
B
Toto
P
P
Feliciani
C
C
Fabbri
P
P
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017302:Annexins; D001327:Autoimmune Diseases / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D001706:Biopsy; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D004817:Epidermis / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D005260:Female; D006098:Granulocytes / Q000473:pathology; D006801:Humans; D007249:Inflammation; D007371:Interferon-gamma / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D015848:Interleukin-5 / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D008297:Male; D008407:Mast Cells / Q000473:pathology; D008875:Middle Aged; D009504:Neutrophils / Q000473:pathology; D010392:Pemphigus / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016037:Single-Blind Method; D012867:Skin / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018418:Th2 Cells / Q000378:metabolism*
C114643:ANXA9 protein, human; D017302:Annexins; D016207:Cytokines; D015848:Interleukin-5; D015850:Interleukin-6; D012333:RNA, Messenger; D015847:Interleukin-4; D007371:Interferon-gamma