PMID- 8675804
OWN - NLM
STAT- MEDLINE
DCOM- 19960815
LR  - 20170214
IS  - 0022-0345 (Print)
IS  - 0022-0345 (Linking)
VI  - 75
IP  - 3
DP  - 1996 Mar
TI  - Induction of lymphocytes cytotoxic to oral epithelial cells by Streptococcus 
      mitis superantigen.
PG  - 927-34
AB  - The preparation of a superantigenic fraction F-2 from the culture supernatant of 
      Streptococcus mitis 108, a fresh isolate from human tooth surfaces, was reported 
      previously. Now, to determine the possible pathogenic role of the superantigen in 
      oral mucosal diseases, we examined the cytotoxic effects of human peripheral 
      blood T-cells activated with F-2 on human oral epithelial cells. T-cells 
      activated with F-2 were cytotoxic to the human squamous carcinoma HO-1-N-1 cells 
      derived from the oral mucosa, similar to those activated with Staphylococcus 
      aureus enterotoxin B (SEB). This cytotoxic effect was increased in a 
      dose-dependent manner by the addition of the respective stimulant, F-2 or SEB, to 
      the cytotoxic assay system. F-2 endowed mainly CD8+ T-cells with cytotoxic 
      activity. Pretreatment with human interferon gamma increased the sensitivity of 
      the HO-1-N-1 cells to the cytotoxic effects of F-2-activated T-cells. The 
      F-2-activated T-cells were also cytotoxic to human keratinocytes derived from 
      gingiva. There was no correlation between the degree of cytotoxicity and the 
      levels of tumor necrosis factor alpha in co-cultures of F-2-activated T-cells and 
      HO-1-N-1 cells. A double-chamber plate experiment revealed no cytotoxic effects 
      when the F-2-activated T-cells were separated from the HO-1-N-1 cells. 
      Supernatants of the co-cultures of target and effector cells were not cytotoxic 
      to HO-1-N-1 cells. These findings suggest that the cytotoxic effects of the 
      F-2-activated T-cells on HO-1-N-1 cells were mediated not by soluble factors but 
      by the direct interaction between the activated T-cells and the target cells. The 
      cytotoxicity of the F-2-activated T-cells against HO-1-N-1 cells was markedly 
      inhibited by monoclonal antibodies (MAbs) against CD11a and CD54, but was only 
      slightly inhibited by MAbs against human leukocyte antigen (HLA)-DR and CD2. 
      Thus, the interaction between lymphocyte-function-associated antigen-1 (LFA-1) 
      and intercellular adhesion molecule-1 (ICAM-1) was crucial for the F-2-dependent 
      T-cell-mediated cytotoxicity against oral epithelial cells, while HLA-DR and CD2 
      molecules are not necessarily involved in the cytotoxicity observed.
FAU - Matsushita, K
AU  - Matsushita K
AD  - Department of Microbiology and Immunology, Kagoshima University Dental School, 
      Japan.
FAU - Sugiyama, A
AU  - Sugiyama A
FAU - Uchiyama, T
AU  - Uchiyama T
FAU - Igarashi, H
AU  - Igarashi H
FAU - Ohkuni, H
AU  - Ohkuni H
FAU - Nagaoka, S
AU  - Nagaoka S
FAU - Kotani, S
AU  - Kotani S
FAU - Takada, H
AU  - Takada H
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Dent Res
JT  - Journal of dental research
JID - 0354343
RN  - 0 (Antigens, Bacterial)
RN  - 0 (Superantigens)
SB  - IM
MH  - Antigens, Bacterial/*immunology
MH  - Carcinoma, Squamous Cell/immunology
MH  - Cells, Cultured
MH  - Cytotoxicity Tests, Immunologic
MH  - Cytotoxicity, Immunologic/immunology
MH  - Dose-Response Relationship, Immunologic
MH  - Epithelial Cells
MH  - Epithelium/immunology
MH  - Gingiva/cytology/*immunology
MH  - Humans
MH  - Infant
MH  - Keratinocytes/immunology
MH  - Lymphocyte Activation/*immunology
MH  - Male
MH  - Mouth Mucosa/cytology/*immunology
MH  - Mouth Neoplasms/immunology
MH  - Streptococcus/*immunology
MH  - Superantigens/*immunology
MH  - T-Lymphocytes, Cytotoxic/*immunology
EDAT- 1996/03/01 00:00
MHDA- 1996/03/01 00:01
CRDT- 1996/03/01 00:00
PHST- 1996/03/01 00:00 [pubmed]
PHST- 1996/03/01 00:01 [medline]
PHST- 1996/03/01 00:00 [entrez]
AID - 10.1177/00220345960750031001 [doi]
PST - ppublish
SO  - J Dent Res. 1996 Mar;75(3):927-34. doi: 10.1177/00220345960750031001.