scholarly journals T lymphocytes and normal tissue responses to radiation

2012 ◽  
Vol 2 ◽  
Author(s):  
Dörthe Schaue ◽  
William H. McBride
Keyword(s):  
T Lymphocytes ◽  
Normal Tissue ◽  
Tissue Responses

scholarly journals Tumor Eradication by Wild-type p53-specific Cytotoxic T Lymphocytes

1997 ◽  
Vol 186 (5) ◽  
pp. 695-704 ◽  
Author(s):  
Michel P.M. Vierboom ◽  
Hans W. Nijman ◽  
Rienk Offringa ◽  
Ellen I.H. van der Voort ◽  
Thorbald van Hall ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Tumor Cells ◽  
Cytotoxic T Lymphocytes ◽  
Normal Tissue ◽  
P53 Protein ◽  
P53 Gene ◽  
Wild Type ◽  
Wild Type P53 ◽  
Tumor Outgrowth ◽  
Tumor Eradication

The tumor suppressor protein p53 is overexpressed in close to 50% of all human malignancies. The p53 protein is therefore an attractive target for immunotherapy. Cytotoxic T lymphocytes (CTLs) recognizing a murine wild-type p53 peptide, presented by the major histocompatibility complex class I molecule H-2Kb, were generated by immunizing p53 gene deficient (p53 −/−) C57BL/6 mice with syngeneic p53-overexpressing tumor cells. Adoptive transfer of these CTLs into tumor-bearing p53 +/+ nude mice caused complete and permanent tumor eradication. Importantly, this occurred in the absence of any demonstrable damage to normal tissue. When transferred into p53 +/+ immunocompetent C57BL/6 mice, the CTLs persisted for weeks in the absence of immunopathology and were capable of preventing tumor outgrowth. Wild-type p53-specific CTLs can apparently discriminate between p53-overexpressing tumor cells and normal tissue, indicating that widely expressed autologous molecules such as p53 can serve as a target for CTL-mediated immunotherapy of tumors.

Ultrastructural study of tumor-infiltrating СD4+ Т-lymphocytes in colon cancer.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e23074-e23074
Author(s):  
Anastasia Grankina ◽  
Elena Yurievna Zlatnik ◽  
Inna Arnoldovna Novikova ◽  
Svetlana Yu. Filippova ◽  
Aleksandr K. Logvinov ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
T Lymphocytes ◽  
Normal Tissue ◽  
Colon Adenocarcinoma ◽  
Tumor Infiltrating Lymphocytes ◽  
Transmission Electron ◽  
Healthy Donors ◽  
Resection Line ◽  
Minimal Damage ◽  
Induced Changes

e23074 Background: The purpose of the study was to assess stress-induced metabolic changes in СD4+ T-lymphocytes among tumor-infiltrating lymphocytes (TILs) according to ultrastructural morphometric parameters. Methods: Samples (n = 12) of colon adenocarcinoma, corresponding resection line tissues and blood of patients and healthy donors were studied. After grinding the samples and PBMC isolation using the density gradient, CD4+ T-lymphocytes separation with magnetic columns was performed using CD4 MicroBeads, human (MACS Miltenyi Biotech). The pellet obtained after centrifugation was embedded in agarose and prepared for transmission electron microscopy. Mitochondria images on ultrathin sections of Т-lymphocytes were randomly selected for the analysis. The total number of mitochondria studied were 71 (tumor), 78 (normal tissue), 78 (blood of patients), 80 (blood of healthy donors). For each image the unchanged cristae area was determined as a percentage of the total area of mitochondria cross section. Results: We found no differences in the structures of mitochondria of blood lymphocytes in patients and in healthy donors. Comparison of parameters of CD4+ Т-lymphocyte mitochondria in the colon unchanged tissues and in the blood of patients did not show significant differences indicating minimal damage during TILs` isolation from the tissues. Electron microscopy of TILs derived from tumor tissue showed more frequent apoptotic and necrotic death of lymphocytes, as well as some mitochondrial swelling with changes in the shape and the number of cristae compared to the norm. Statistical analysis revealed significant decrease in the relative area of unchanged cristae: 57% in tumor against 73% in the normal tissue (p < 0.0001, χ2Test). Conclusions: The results suggest that stress-induced changes are developed in tumor-infiltrating CD4+ T-lymphocytes, and these changes apparently enhance their death as demonstrated by ultrastructural characteristics of mitochondria.

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