Enhanced peripheral blood T-cell cytotoxicity in inflammatory bowel disease

Typeset version

 

TY  - JOUR
  - Shanahan, F.,Leman, B.,Deem, R.,Niederlehner, A.,Brogan, M.,Targan, S.
  - 1989
  - January
  - J Clin Immunolj Clin Immunol
  - Enhanced peripheral blood T-cell cytotoxicity in inflammatory bowel disease
  - Validated
  - ()
  - 9
  - 11
  - 55
  - 64
  - Monoclonal antibodies to the CD3 component of the T-cell antigen receptor can trigger antigen-specific cytotoxic T cells to elicit nonantigen-specific cytotoxicity, possibly by mimicking or bypassing the requirement for antigen triggering. We have used this technique to investigate the possible presence of in vivo primed cytotoxic T cells, of unknown antigen specificity, in peripheral blood of patients with inflammatory bowel disease. Peripheral blood lymphocytes, which were depleted of background natural killer (NK) activity (CD16-), from patients with Crohn's disease exhibited significantly enhanced levels of anti-CD3-triggered T-cell cytotoxicity compared with lymphocytes from normal subjects. Enhanced lytic activity was also found in some patients with ulcerative colitis and in patients with ulcerative colitis postcolectomy. These results were not influenced by treatment or disease activity. There was no correlation between the anti-CD3-triggered T lytic activity and the NK activity in normal subjects or in patients with inflammatory bowel disease. The surface antigen phenotype of the anti-CD3-triggered T killer cell was CD3+, CD8+, CD16-, and Leu 7+. The results provide indirect evidence for increased activity of a subpopulation of cytotoxic T cells, of unknown antigen specificity, in inflammatory bowel disease. Increased activity in patients with ulcerative colitis postcolectomy suggests that this might reflect a fundamental immunological disturbance.Monoclonal antibodies to the CD3 component of the T-cell antigen receptor can trigger antigen-specific cytotoxic T cells to elicit nonantigen-specific cytotoxicity, possibly by mimicking or bypassing the requirement for antigen triggering. We have used this technique to investigate the possible presence of in vivo primed cytotoxic T cells, of unknown antigen specificity, in peripheral blood of patients with inflammatory bowel disease. Peripheral blood lymphocytes, which were depleted of background natural killer (NK) activity (CD16-), from patients with Crohn's disease exhibited significantly enhanced levels of anti-CD3-triggered T-cell cytotoxicity compared with lymphocytes from normal subjects. Enhanced lytic activity was also found in some patients with ulcerative colitis and in patients with ulcerative colitis postcolectomy. These results were not influenced by treatment or disease activity. There was no correlation between the anti-CD3-triggered T lytic activity and the NK activity in normal subjects or in patients with inflammatory bowel disease. The surface antigen phenotype of the anti-CD3-triggered T killer cell was CD3+, CD8+, CD16-, and Leu 7+. The results provide indirect evidence for increased activity of a subpopulation of cytotoxic T cells, of unknown antigen specificity, in inflammatory bowel disease. Increased activity in patients with ulcerative colitis postcolectomy suggests that this might reflect a fundamental immunological disturbance.
  - 0271-9142 (Print) 0271-91
DA  - 1989/01
ER  - 
@article{V280546293,
   = {Shanahan,  F. and Leman,  B. and Deem,  R. and Niederlehner,  A. and Brogan,  M. and Targan,  S. },
   = {1989},
   = {January},
   = {J Clin Immunolj Clin Immunol},
   = {Enhanced peripheral blood T-cell cytotoxicity in inflammatory bowel disease},
   = {Validated},
   = {()},
   = {9},
   = {11},
  pages = {55--64},
   = {{Monoclonal antibodies to the CD3 component of the T-cell antigen receptor can trigger antigen-specific cytotoxic T cells to elicit nonantigen-specific cytotoxicity, possibly by mimicking or bypassing the requirement for antigen triggering. We have used this technique to investigate the possible presence of in vivo primed cytotoxic T cells, of unknown antigen specificity, in peripheral blood of patients with inflammatory bowel disease. Peripheral blood lymphocytes, which were depleted of background natural killer (NK) activity (CD16-), from patients with Crohn's disease exhibited significantly enhanced levels of anti-CD3-triggered T-cell cytotoxicity compared with lymphocytes from normal subjects. Enhanced lytic activity was also found in some patients with ulcerative colitis and in patients with ulcerative colitis postcolectomy. These results were not influenced by treatment or disease activity. There was no correlation between the anti-CD3-triggered T lytic activity and the NK activity in normal subjects or in patients with inflammatory bowel disease. The surface antigen phenotype of the anti-CD3-triggered T killer cell was CD3+, CD8+, CD16-, and Leu 7+. The results provide indirect evidence for increased activity of a subpopulation of cytotoxic T cells, of unknown antigen specificity, in inflammatory bowel disease. Increased activity in patients with ulcerative colitis postcolectomy suggests that this might reflect a fundamental immunological disturbance.Monoclonal antibodies to the CD3 component of the T-cell antigen receptor can trigger antigen-specific cytotoxic T cells to elicit nonantigen-specific cytotoxicity, possibly by mimicking or bypassing the requirement for antigen triggering. We have used this technique to investigate the possible presence of in vivo primed cytotoxic T cells, of unknown antigen specificity, in peripheral blood of patients with inflammatory bowel disease. Peripheral blood lymphocytes, which were depleted of background natural killer (NK) activity (CD16-), from patients with Crohn's disease exhibited significantly enhanced levels of anti-CD3-triggered T-cell cytotoxicity compared with lymphocytes from normal subjects. Enhanced lytic activity was also found in some patients with ulcerative colitis and in patients with ulcerative colitis postcolectomy. These results were not influenced by treatment or disease activity. There was no correlation between the anti-CD3-triggered T lytic activity and the NK activity in normal subjects or in patients with inflammatory bowel disease. The surface antigen phenotype of the anti-CD3-triggered T killer cell was CD3+, CD8+, CD16-, and Leu 7+. The results provide indirect evidence for increased activity of a subpopulation of cytotoxic T cells, of unknown antigen specificity, in inflammatory bowel disease. Increased activity in patients with ulcerative colitis postcolectomy suggests that this might reflect a fundamental immunological disturbance.}},
  issn = {0271-9142 (Print) 0271-91},
  source = {IRIS}
}
AUTHORSShanahan, F.,Leman, B.,Deem, R.,Niederlehner, A.,Brogan, M.,Targan, S.
YEAR1989
MONTHJanuary
JOURNAL_CODEJ Clin Immunolj Clin Immunol
TITLEEnhanced peripheral blood T-cell cytotoxicity in inflammatory bowel disease
STATUSValidated
TIMES_CITED()
SEARCH_KEYWORD
VOLUME9
ISSUE11
START_PAGE55
END_PAGE64
ABSTRACTMonoclonal antibodies to the CD3 component of the T-cell antigen receptor can trigger antigen-specific cytotoxic T cells to elicit nonantigen-specific cytotoxicity, possibly by mimicking or bypassing the requirement for antigen triggering. We have used this technique to investigate the possible presence of in vivo primed cytotoxic T cells, of unknown antigen specificity, in peripheral blood of patients with inflammatory bowel disease. Peripheral blood lymphocytes, which were depleted of background natural killer (NK) activity (CD16-), from patients with Crohn's disease exhibited significantly enhanced levels of anti-CD3-triggered T-cell cytotoxicity compared with lymphocytes from normal subjects. Enhanced lytic activity was also found in some patients with ulcerative colitis and in patients with ulcerative colitis postcolectomy. These results were not influenced by treatment or disease activity. There was no correlation between the anti-CD3-triggered T lytic activity and the NK activity in normal subjects or in patients with inflammatory bowel disease. The surface antigen phenotype of the anti-CD3-triggered T killer cell was CD3+, CD8+, CD16-, and Leu 7+. The results provide indirect evidence for increased activity of a subpopulation of cytotoxic T cells, of unknown antigen specificity, in inflammatory bowel disease. Increased activity in patients with ulcerative colitis postcolectomy suggests that this might reflect a fundamental immunological disturbance.Monoclonal antibodies to the CD3 component of the T-cell antigen receptor can trigger antigen-specific cytotoxic T cells to elicit nonantigen-specific cytotoxicity, possibly by mimicking or bypassing the requirement for antigen triggering. We have used this technique to investigate the possible presence of in vivo primed cytotoxic T cells, of unknown antigen specificity, in peripheral blood of patients with inflammatory bowel disease. Peripheral blood lymphocytes, which were depleted of background natural killer (NK) activity (CD16-), from patients with Crohn's disease exhibited significantly enhanced levels of anti-CD3-triggered T-cell cytotoxicity compared with lymphocytes from normal subjects. Enhanced lytic activity was also found in some patients with ulcerative colitis and in patients with ulcerative colitis postcolectomy. These results were not influenced by treatment or disease activity. There was no correlation between the anti-CD3-triggered T lytic activity and the NK activity in normal subjects or in patients with inflammatory bowel disease. The surface antigen phenotype of the anti-CD3-triggered T killer cell was CD3+, CD8+, CD16-, and Leu 7+. The results provide indirect evidence for increased activity of a subpopulation of cytotoxic T cells, of unknown antigen specificity, in inflammatory bowel disease. Increased activity in patients with ulcerative colitis postcolectomy suggests that this might reflect a fundamental immunological disturbance.
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ISBN_ISSN0271-9142 (Print) 0271-91
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