Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Although it is known that the immune system can mount responses to a variety of tumors it is clear that most tumors exhibit weak or even undetectable immunogenicity. Recent findings suggest that the lack of tumor immunogenicity is partly due to a population of cells called CD4+ CD25+ regulatory T cells since depletion of these cells in mice can result in tumor rejection. These cells have also been shown to inhibit the development of organ-specific autoimmune diseases suggesting that they inhibit immune responses to tissue-specific self-antigens. Such immune responses may also mediate tumor rejection. Alternatively, immune responses in mice depleted of regulatory cells may target tumor antigens that are not tissue-specific, but which are shared by tumors of diverse origins. In experiments performed to discriminate between these possibilities we found, using the murine colorectal tumor CT26, that tumor immunity stimulated in the absence of regulatory cells is not restricted to tumors of colorectal origin, but is effective against tumors of different histological types such as B cell lymphomas and a renal cell carcinoma. By comparing this to CT26-induced immunity through the use of adjuvant we show that the generation of cross-reactive tumor immunity is a specific manifestation of CD25+ regulatory cell depletion. The generation of CD4+ T cells capable of mediating tumor rejection is another important feature of tumor immunity induced in the absence of CD25+ cells.

Original publication

DOI

10.1002/1521-4141(200211)32:11<3267::aid-immu3267>3.0.co;2-1

Type

Journal article

Journal

European journal of immunology

Publication Date

11/2002

Volume

32

Pages

3267 - 3275

Addresses

Cancer Sciences Division, University of Southampton School of Medicine, Southampton, GB.

Keywords

T-Lymphocytes, CD4-Positive T-Lymphocytes, Animals, Mice, Inbred BALB C, Mice, Colonic Neoplasms, Receptors, Interleukin-2, Cancer Vaccines, Antigens, Neoplasm, Lymphocyte Depletion, Cross Reactions