The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
CD4 T Cells and Their Role in Antitumor Immune Responses
Open accessAbstract
The specificity and power of the cellular arm of the immune system may provide new therapeutic approaches to cancer. With the assumption that T cells might be able to recognize and eliminate cancer cells with the same efficiency as virus-infected cells, investigators have searched many years for ways to trigger or amplify the patient's inadequate immune response to tumors. Much attention has been given to the role of CD8+ CTLs because most tumors are MHC class I positive, but negative for MHC class II. Moreover, CD8+ CTLs are able to lyse tumor cells directly upon recognition of peptide–MHC class I complexes expressed by the tumor, and their ability to eradicate large tumor masses in vivo has been demonstrated. The focus in cancer immunology on CD8+ T cell responses is also exemplified by an increasing list of tumor antigens identified by tumor-reactive CD8+ CTLs. CD4+ Th cells have received far less attention, which is remarkable given the pivotal role of these cells in regulating most antigen-specific immune responses. Until now, only a few Th epitopes derived from human tumor antigens recognized by CD4+ Th cells have been identified (1, 2). Three studies published in this issue describe the identification of melanoma antigens that are recognized by CD4+ T cells in the context of MHC class II molecules (3–5). Charting the Th response against human melanoma as well as other tumors is important for the development of optimal anticancer vaccines and for the design of other T cell–related therapeutic modalities in cancer.
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Cites
T-cell help for cytotoxic T lymphocytes is mediated by CD40–CD40L interactions
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Self-citationA conditioned dendritic cell can be a temporal bridge between a CD4+ T-helper and a T-killer cell
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The Central Role of CD4+ T Cells in the Antitumor Immune Response
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Role of Bone Marrow-Derived Cells in Presenting MHC Class I-Restricted Tumor Antigens
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Cited by
Bell, D., Chomarat, P., Broyles, D., Netto, G., Harb, G. M., Lebecque, S., Valladeau, J., Davoust, J., Palucka, K. A., & Banchereau, J. (1999) · The Journal of Experimental Medicine · doi:10.1084/jem.190.10.1417 · Cited by 544
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Yu, P., Lee, Y., Liu, W., Krausz, T., Chong, A., Schreiber, H., & Fu, Y.-X. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041684 · Cited by 432
Su, Z., Dannull, J., Yang, B. K., Dahm, P., Coleman, D., Yancey, D., Sichi, S., Niedzwiecki, D., Boczkowski, D., Gilboa, E., et al. (2005) · The Journal of Immunology · doi:10.4049/jimmunol.174.6.3798 · Cited by 359
Chronic Stress and Susceptibility to Skin Cancer
Saul, A. N., Oberyszyn, T. M., Daugherty, C., Kusewitt, D., Jones, S., Jewell, S., Malarkey, W. B., Lehman, A., Lemeshow, S., & Dhabhar, F. S. (2005) · JNCI: Journal of the National Cancer Institute · doi:10.1093/jnci/dji401 · Cited by 245
Metadata
- Authors
- Toes, R. E. M., Ossendorp, F., Offringa, R., & Melief, C. J. M.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 1999-03-01
- Volume
- 189
- Issue
- 5
- Pages
- 753-756
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2040594411
- Cited by
- 508
- References
- 36
- FWCI
- 14.74
- Type
- journal article
- Language
- en
- Open access
- green
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