In:
Immunology & Cell Biology, Wiley, Vol. 83, No. 4 ( 2005-08), p. 344-351
Kurzfassung:
4‐1BB costimulates T cells to carry out effector functions such as eradication of established tumours. 4‐1BB (CD137) is a member of the TNF receptor family, and its triggering by either 4‐1BB ligand or antibody ligation induces T‐cell activation and growth. We analysed tumour‐infiltrating lymphocytes (TIL) in the experimental B16F10 melanoma model to determine the mechanisms involved in 4‐1BB‐mediated tumour suppression. 4‐1BB +/+ mice survived longer than 4‐1BB –/– mice, and survival was further prolonged by triggering 4‐1BB with an agonistic mAb. The number of metastatic B16F10 colonies in the lung was much greater in 4‐1BB –/– mice than in their 4‐1BB +/+ littermates. Administration of agonistic anti‐4‐1BB mAb increased the number of TIL in the tumour masses in the lungs of 4‐1BB +/+ mice. The numbers of CD4 + T, CD8 + T and CD11b + TIL increased in these mice. Anti‐4‐1BB mAb induced not only CD8 + 4‐1BB + T cells but also a CD8 + IFN‐γ + T‐cell population. B16F10 cells from the lungs of anti‐4‐1BB‐treated mice showed enhanced expression of MHC class Ι and II antigens compared with the same cells from control IgG‐treated mice. Thus, the increase in number of CD8 + T cells and enhanced MHC Ι and II expression in B16F10 cells that result from augmented IFN‐γ production in response to anti‐4‐1BB mAb may lead to suppression of tumour growth and metastasis.
Materialart:
Online-Ressource
ISSN:
0818-9641
,
1440-1711
DOI:
10.1111/imcb.2005.83.issue-4
DOI:
10.1111/j.1440-1711.2005.01330.x
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2005
ZDB Id:
2011707-3
SSG:
12