Proliferative activity of CD8(+) T cells as an important clue to analyze T cell-mediated inflammatory dermatoses.
To elucidate the pathogenesis of T cell-mediated inflammatory skin diseases, we examined the exact sites where CD8(+) T cells proliferate, correlating them with the localization of antigen-presenting dendritic cells. We performed CD8/Ki-67 double immunohistochemical staining and single staining for CD1a, CD68, and factor XIIIa on sections of paraffin-embedded tissue samples of inflammatory dermatoses in which T lymphocytes are thought to play a crucial role. The dermatoses were lichen planus (12 samples), acute graft-versus host disease (GVHD) (12 samples), chronic GVHD (10 samples), spongiotic dermatitis (8 samples) and psoriasis (7 samples). Labelling for Ki-67 among CD8(+) T cells was predominantly observed in the subepidermal lymphoid infiltrate, and was scanty in the epidermis. This suggested that proliferation of CD8(+) T cells occurred preferentially in the dermis. The labelling index for Ki-67 among dermal and epidermal CD8(+) cells was quite different among the different diseases studied (P < 0.05). They were rich in the subepidermal portion of the dermis of spongiotic dermatitis, acute GVHD and chronic GVHD, but rare in the dermis of psoriasis and lichen planus. A moderate infiltrate was also observed in lesional epidermis of spongiotic dermatitis, acute GVHD and chronic GVHD, whereas they was almost none in the epidermis of psoriasis and lichen planus. CD1a(+) dermal dendritic cells were densely distributed within the lymphoid infiltrate in the affected dermis of spongiotic dermatitis, psoriasis and lichen planus, whereas they were minimal in GVHD. These dermal dendritic cells are candidates as stimulators on T cells in the dermis. In conclusion, the proliferative status of T cells could be an important clue in the elucidation of the pathophysiology of T cell-mediated inflammatory dermatoses.
Deguchi
M
M
Department of Dermatology, Tohoku University School of Medicine, Sendai, Japan.
Ohtani
H
H
Sato
E
E
Naito
Y
Y
Nagura
H
H
Aiba
S
S
Tagami
H
H
D000208:Acute Disease; D018949:Antigens, CD1 / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000473:pathology* / Q000502:physiology*; D002455:Cell Division; D002908:Chronic Disease; D003713:Dendritic Cells / Q000378:metabolism; D006086:Graft vs Host Disease / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D019394:Ki-67 Antigen / Q000378:metabolism; D008010:Lichen Planus / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D011565:Psoriasis / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D012867:Skin / Q000378:metabolism / Q000473:pathology; D012871:Skin Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D013194:Staining and Labeling; D014018:Tissue Distribution
D018949:Antigens, CD1; C419393:CD1a antigen; D019394:Ki-67 Antigen