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Recognition of adult T-cell leukemia/lymphoma cells by CD4+ helper T lymphocytes specific for human T-cell leukemia virus type I envelope protein

  • Hiroya Kobayashi(corresponding author)
    ,
  • Toshihiro Nagato
    ,
  • Mitsuru Yanai
    ,
  • Kensuke Oikawa
    ,
  • Keisuke Sato
    ,
  • Shoji Kimura
*Corresponding author for this work
  • Asahikawa Medical University
    ,
  • Mayo Clinic College of Medicine and Science
Scholary Output:
Contribution to journal
Article
Peer-review

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Purpose: Human T-cell leukemia virus type I (HTLV-I) can cause an adult T-cell leukemia/lymphoma (ATLL). Because ATLL is a life-threatening lymphoproliferative disorder and is resistant to chemotherapy, the establishment and enhancement of T-cell immunity to HTLV-I through the development of therapeutic vaccines could be of value. Thus, the identification of HTLV-I epitopes for both CD8+ and CD4+ T cells should facilitate the development of effective vaccines. Although numerous HTLV-I epitopes for CTLs have been identified, few epitopes recognized by CD4+ helper T cells against this virus have been described. Experimental Design: Synthetic peptides prepared from several regions of the HTLV-I envelope (Env) sequence that were predicted to serve as helper T-cell epitopes were prepared with use of computer-based algorithms and tested for their capacity to trigger in vitro helper T-cell responses using lymphocytes from normal volunteers. Results: The results show that the HTLV-I-Env317-331, and HTLV-I-Env 384-398-reactive helper T lymphocytes restricted by HLA-DQw6 and HLA-DR15, respectively, could recognize intact HTLV-I+ T-cell lymphoma cells and, as a consequence, secrete lymphokines. In addition, HTLV-I Env 196-210-reactive helper T lymphocytes restricted by HLA-DR9 were able to directly kill HTLV-I+ lymphoma cells and recognize naturally processed antigen derived from killed HTLV-I+ lymphoma cells, which was presented to the helper T cells by autologous antigen-presenting cells. Conclusions: The present findings hold relevance for the design and optimization of T-cell epitope-based immunotherapy against HTLV-I-induced diseases such as ATLL.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 7053-7062 (10 pages)

Journal (Volume, Issue Number)

Clinical Cancer Research (Volume 10, Issue 20)

Publication milestones

  • Published - 10/15/2004

Publication status

Published - 10/15/2004

ISSN

1078-0432

Publication IDs

  • Scopus: 6044233329
  • PubMed: 15501985

Publication metrics

Metrics

Scopus
citations
Fractional count
1
Fractional count
0.11
Fractional count
8
Fractional count
0.89
Fractional count
1
Fractional count
1
SciVal
FWCI
0.45
SciVal
Author count
9
SciVal
citations
10
SciVal
Paper percentile
58

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Captures
12
Citation count
11

Funding Details

FunderFunding number
NCI
P50CA091956