Immunity and Immune Suppression in Human Ovarian Cancer

Abstract

Clinical outcomes in ovarian cancer are heterogeneous, independent of common features such as stage, response to therapy and grade. This disparity in outcomes warrants further exploration into tumor and host characteristics. One compelling issue is the response of the patient‘s immune system to her ovarian cancer. Several studies have confirmed a prominent role for the immune system in modifying disease course. This has led to the identification and evaluation of novel immune-modulating therapeutic approaches such as vaccination and antibody therapy. Antitumor immunity, however, is often negated by immune suppression mechanisms present in the tumor microenvironment. Thus, in the future, research into immunotherapy targeting ovarian cancer will probably become increasingly focused on combination approaches that simultaneously augment immunity while preventing local immune suppression. In this article, we summarize important immunological issues that could influence ovarian cancer outcome, including tumor antigens, endogenous immune responses, immune escape and new and developing immunotherapeutic strategies.

KEYWORDS::

• antibody therapy
• myeloid-derived suppressor cells
• regulatory T cells
• vaccines

Financial & competing interests disclosure

Work on ovarian cancers in the authors‘ laboratories is supported by the Minnesota Ovarian Cancer Alliance (Keith L Knutson), the Fred C and Katherine B Andersen Foundation (Keith L Knutson and Kimberly R Kalli), R01-CA122443 (to Ellen L Goode) and the Mayo Clinic Ovarian Cancer SPORE (P50-CA136393 to Lynn C Hartmann, Keith L Knutson and Ellen L Goode). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

Work on ovarian cancers in the authors‘ laboratories is supported by the Minnesota Ovarian Cancer Alliance (Keith L Knutson), the Fred C and Katherine B Andersen Foundation (Keith L Knutson and Kimberly R Kalli), R01-CA122443 (to Ellen L Goode) and the Mayo Clinic Ovarian Cancer SPORE (P50-CA136393 to Lynn C Hartmann, Keith L Knutson and Ellen L Goode). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.