Research ArticleCancer

Agonism of CD11b reprograms innate immunity to sensitize pancreatic cancer to immunotherapies

See allHide authors and affiliations

Science Translational Medicine  03 Jul 2019:
Vol. 11, Issue 499, eaau9240
DOI: 10.1126/scitranslmed.aau9240

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Manipulating myeloid cells through CD11b

Attempts to alter the phenotype or remove suppressive myeloid cells from the tumor microenvironment are working their way to the clinic. Panni et al. tested a small-molecule agonist of the integrin CD11b to mitigate myeloid cell immunosuppression in mouse models of pancreatic ductal adenocarcinoma. This drug, ADH-503, reduced myeloid cell recruitment and altered the phenotypes of myeloid cells within the tumor. ADH-503 treatment increased responses to chemotherapy or radiation and also rendered normally resistant tumors sensitive to checkpoint blockade, as T cell phenotypes and recruitment were also modified indirectly. These exciting results show how targeting an integrin on myeloid cells could improve treatment for a devastating cancer type.

View Full Text