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A spontaneously arising pancreatic tumor does not promote the differentiation of naive CD8+ T lymphocytes into effector CTL

Academic Article
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Overview

authors

  • Lyman, M. A.
  • Aung, S.
  • Biggs, J. A.
  • Sherman, Linda

publication date

  • June 2004

journal

  • Journal of Immunology  Journal

abstract

  • In this report, we address whether a growing tumor provides sufficient inflammatory signals to promote activation, clonal expansion, and acquisition of effector functions by naive tumor-specific CD8(+) T lymphocytes. CD8(+) T lymphocytes obtained from hemagglutinin (HA)-specific clone 4 TCR-transgenic mice were injected into recipient mice that spontaneously develop pancreatic tumors expressing HA as a tumor-associated Ag (RIP-Tag2-HA mice). When 3 x 10(6) clone 4 CD8(+) T cells were transferred into tumor-bearing mice, the cells became activated in the pancreatic lymph nodes where they proliferated and acquired effector functions such as cytolytic activity and IFN-gamma production. Surprisingly, reducing the number of adoptively transferred CD8(+) T cells led to a parallel reduction in the proportion of the activated cells that exhibited effector functions, suggesting that CTL differentiation was induced by the large numbers of activated CD8(+) T cells and not the tumor environment. Provision of tumor-specific CD4(+) helper cells provided the signals required to promote both the development of CTL effector functions and increased clonal expansion, resulting in tumor eradication. Considering that only small numbers of tumor-specific CD8(+) T cells would be present in a conventional T cell repertoire, these data suggest that tumor growth alone may not provide the inflammatory signals necessary to support the development of CD8(+) T cell effector functions.

subject areas

  • Adoptive Transfer
  • Animals
  • Antigens, Polyomavirus Transforming
  • CD4-Positive T-Lymphocytes
  • CD8-Positive T-Lymphocytes
  • Cell Differentiation
  • Cell Line
  • Hemagglutinin Glycoproteins, Influenza Virus
  • Insulin
  • Mice
  • Mice, Inbred C57BL
  • Pancreatic Neoplasms
  • Promoter Regions, Genetic
  • Rats
  • Receptors, Antigen, T-Cell
  • T-Lymphocytes, Cytotoxic
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 15153470
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Additional Document Info

start page

  • 6558

end page

  • 6567

volume

  • 172

issue

  • 11

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