Journal
IMMUNOLOGICAL INVESTIGATIONS
Volume 41, Issue 6-7, Pages 614-634Publisher
TAYLOR & FRANCIS INC
DOI: 10.3109/08820139.2012.680634
Keywords
MDSC; tumor immunology; arginine
Categories
Funding
- NCI NIH HHS [R01 CA082689, R01 CA107974, R21 CA162133] Funding Source: Medline
- NIGMS NIH HHS [P20 GM103501] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA082689, R01CA107974, R21CA162133] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P20GM103501] Funding Source: NIH RePORTER
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Patients with cancer have an impaired T cell response that can decrease the potential therapeutic benefit of cancer vaccines and other forms of immunotherapy. The establishment of a chronic inflammatory environment in patients with cancer plays a critical role in the induction of T cell dysfunction. The accumulation of myeloid-derived suppressor cells (MDSC) in tumor bearing hosts is a hallmark of malignancy-associated inflammation and a major mediator of the induction of T cell suppression in cancer. Recent findings in tumor bearing mice and cancer patients indicate that the increased metabolism of L-Arginine (L-Arg) by MDSC producing Arginase I inhibits T cell lymphocyte responses. Here, we discuss some of the most recent concepts of how MDSC expressing Arginase I may regulate T cell function in cancer and suggest possible therapeutic interventions to overcome this inhibitory effect.
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