PMID- 15664948
OWN - NLM
STAT- MEDLINE
DCOM- 20050311
LR  - 20181113
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 73
IP  - 2
DP  - 2005 Feb
TI  - Expression of major histocompatibility complex class II and CD80 by gingival 
      epithelial cells induces activation of CD4+ T cells in response to bacterial 
      challenge.
PG  - 1044-51
AB  - HLA-DR (major histocompatibility complex [MHC] class II) is often expressed by 
      epithelial cells in gingival tissues with periodontal disease but not by cells in 
      healthy gingival tissues. Confocal microscopic analyses revealed that gingival 
      epithelial cells (GEC) from tissue with periodontal disease express both HLA-DR 
      and B7-1 (CD80) costimulatory molecules. Rat GEC lines were established to 
      elucidate the possible role of MHC class II and B7-1 expression by GEC. 
      Stimulation of a rat GEC line with gamma interferon (IFN-gamma) induced the 
      expression of MHC class II, whereas the cell line constitutively expressed B7-1 
      costimulatory molecules as determined by reverse transcription-PCR and flow 
      cytometry. Actinobacillus actinomycetemcomitans Omp29-specific CD4(+) Th1 clone 
      cells proliferated in response to pretreatment of GEC with fixed A. 
      actinomycetemcomitans and IFN-gamma. However, the Th1 cells did not respond to 
      pretreatment of GEC with the bacteria alone or IFN-gamma alone. The activation of 
      Th1 clone cells induced by the GEC was inhibited by antibody to MHC class II or 
      by CTLA4 immunoglobulin (CTLA4-Ig). Lymph node T cells did not demonstrate 
      superantigen activity to A. actinomycetemcomitans, although both lymph node T 
      cells and Th1 clone cells were sensitive to superantigen activity of 
      staphylococcal enterotoxin A as cultured in the presence of IFN-gamma-treated 
      GEC. These results suggested that GEC can take up bacterial antigen and 
      consequently process and present the bacterial antigen to CD4(+) T cells by MHC 
      class II in conjunction with B7 costimulation. GEC appeared to play a role in the 
      adaptive immune response by stimulating antigen-specific CD4(+) T cells.
FAU - Matsuyama, Takashi
AU  - Matsuyama T
AD  - Department of Immunology, The Forsyth Institute, 140 The Fenway, Boston, MA 
      02115-3799, USA.
FAU - Kawai, Toshihisa
AU  - Kawai T
FAU - Izumi, Yuichi
AU  - Izumi Y
FAU - Taubman, Martin A
AU  - Taubman MA
LA  - eng
GR  - DE 14551/DE/NIDCR NIH HHS/United States
GR  - R01 DE003420/DE/NIDCR NIH HHS/United States
GR  - DE 03420/DE/NIDCR NIH HHS/United States
GR  - R37 DE003420/DE/NIDCR NIH HHS/United States
GR  - K22 DE014551/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (B7-1 Antigen)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Superantigens)
SB  - IM
MH  - Actinobacillus Infections/immunology
MH  - Aggregatibacter actinomycetemcomitans/immunology
MH  - Animals
MH  - Antigen Presentation/*immunology
MH  - B7-1 Antigen/genetics/*immunology
MH  - CD4-Positive T-Lymphocytes/*immunology
MH  - Chronic Disease
MH  - Epithelial Cells/*immunology
MH  - Gingiva/*immunology
MH  - HLA-DR Antigens/immunology
MH  - Histocompatibility Antigens Class II/*immunology
MH  - Humans
MH  - Periodontitis/immunology
MH  - Rats
MH  - Superantigens/immunology
PMC - PMC546936
EDAT- 2005/01/25 09:00
MHDA- 2005/03/12 09:00
PMCR- 2005/02/01
CRDT- 2005/01/25 09:00
PHST- 2005/01/25 09:00 [pubmed]
PHST- 2005/03/12 09:00 [medline]
PHST- 2005/01/25 09:00 [entrez]
PHST- 2005/02/01 00:00 [pmc-release]
AID - 73/2/1044 [pii]
AID - 0583-04 [pii]
AID - 10.1128/IAI.73.2.1044-1051.2005 [doi]
PST - ppublish
SO  - Infect Immun. 2005 Feb;73(2):1044-51. doi: 10.1128/IAI.73.2.1044-1051.2005.