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. 2014 Jul-Aug;20(4):254-5.
doi: 10.1097/PPO.0000000000000062.

From the guest editor: Tumor site immune modulation therapy

Lieping Chen  1
Affiliations

From the guest editor: Tumor site immune modulation therapy

Lieping Chen. Cancer J. 2014 Jul-Aug.
No abstract available

PubMed Disclaimer

Conflict of interest statement

The author declares no conflict of interest.

Figures

Figure 1
Figure 1
The B7-H1/PD-1 immune modulatory pathway. Five molecules are found in this pathway. B7-H1 (PD-L1) binds PD-1 as a major ligand to transmit a T cell–suppressive signal. In addition, B7-H1 could also interact with CD80 to inhibit T cell responses. Note here that B7-H1 could also act as a receptor to deliver an antiapoptotic signal to tumor cells or antigen-presenting cells. B7-DC (PD-L2) also interacts with PD-1 with affinity that is similar to B7-H1, while the function of this interaction in the regulation of immunity in vivo is less clear. B7-DC binds RGMb to participate in respiratory tolerance.
Figure 2
Figure 2
Induction of immune responses to cancer. During the growth of cancer, tumor antigens are released and presented by professional antigen-presenting cells (APCs). After migration to lymphoid organs, the APCs stimulate activation of naive T cells, and this process is regulated by costimulation and coinhibition. Successful antigen presentation and costimulation lead to generation of effector T cells (Te), which, after they exit lymphoid organs, reach tumor sites to execute effector functions, and a small fraction of Te become long-term memory T cells (Tm). The strategies to stimulate tumor immunity include (1) cancer vaccines that enhance antigen presentation; (2) checkpoint blockades (anti–CTLA-4) and/or enhanced costimulation to systemically amplify T cell activation; (3) adoptive transfer of activated or genetically engineered T cells to provide more Te; and (4) tumor site immune modulation to prevent B7-H1/PD-1 pathway–mediated suppression.
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References

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