Involvement of granulysin-producing T cells in the development of superficial microbial folliculitis.
BACKGROUND
Granulysin is a recently identified antimicrobial protein expressed on cytotoxic T cells, natural killer (NK) cells and NKT cells. It has been shown that granulysin contributes to the defence mechanisms against mycobacterial infection. Superficial microbial folliculitis is a common skin disease. In a previous report, we showed that, as a first line of defence, alpha-defensin, a human neutrophil peptide, and beta-defensin (human beta-defensin-2) were expressed in infiltrating neutrophils and in lesional epidermal keratinocytes, respectively, in superficial folliculitis. As we also observed many infiltrating lymphocytes in lesional dermis, we hypothesized that infiltrating lymphocytes may possess antimicrobial substances, such as granulysin, and play a role in the defence mechanism as a second line of defence.


OBJECTIVE
Seven specimens of superficial microbial folliculitis diagnosed clinically and histologically were examined by means of immunohistochemistry. To identify the phenotype of cells expressing granulysin, confocal laser microscopic examination was performed.


RESULTS
A dense lymphoid cell infiltrate was observed in pustules, in the perivascular regions. A large number of these lymphoid cells were positive for granulysin. Phenotypically, cells consisted of CD3+ T cells, CD8+ T cells and UCHL-1+ T cells. CD20+ cells and CD56+ cells were not observed. Microscopic examination with a confocal laser showed that the lymphocytes producing granulysin were CD3+ and CD4+ T cells but not CD8+ T cells.


CONCLUSIONS
We showed that many granulysin-bearing T cells infiltrated affected follicles and perilesional dermis in superficial microbial folliculitis. However, few granulysin-positive lymphoid cells were observed in sterile pustular lesions. Our observations indicated that adaptive immunity such as granulysin, a lymphocyte-produced antimicrobial protein, may play an important role in the cutaneous defence mechanism.
Oono
T
T
Department of Dermatology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan. otakashi@cc.okayama-u.ac.jp
Morizane
S
S
Yamasaki
O
O
Shirafuji
Y
Y
Huh
W-K
WK
Akiyama
H
H
Iwatsuki
K
K
D000328:Adult; D000368:Aged; D000945:Antigens, Differentiation, T-Lymphocyte; D001424:Bacterial Infections / Q000276:immunology* / Q000473:pathology; D017252:CD3 Complex / Q000032:analysis; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D005260:Female; D005499:Folliculitis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D006801:Humans; D016130:Immunophenotyping; D017493:Leukocyte Common Antigens / Q000032:analysis; D008297:Male; D018613:Microscopy, Confocal; D008875:Middle Aged; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000276:immunology; D012867:Skin / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology*
D000945:Antigens, Differentiation, T-Lymphocyte; D017252:CD3 Complex; C075005:GNLY protein, human; D011971:Receptors, Immunologic; D017493:Leukocyte Common Antigens