Abstract:
:Immune checkpoint immunotherapy is a pillar of human oncology treatment with potential for non-human species. The first checkpoint immunotherapy approved for human cancers targeted the CTLA4 protein. CTLA4 can inhibit T cell activation by capturing and internalizing CD80 and CD86 from antigen presenting cells, a process called trans-endocytosis. Similarly, CD28 can capture CD80 and CD86 via trogocytosis and retain the captured ligands on the surface of the CD28-expressing cells. The wild Tasmanian devil (Sarcophilus harrisii) population has declined by 77% due to transmissible cancers that evade immune defenses despite genetic mismatches between the host and tumors. We used a live cell-based assay to demonstrate that devil CTLA4 and CD28 can capture CD80 and CD86. Mutation of evolutionarily conserved motifs in CTLA4 altered functional interactions with CD80 and CD86 in accordance with patterns observed in other species. These results suggest that checkpoint immunotherapies can be translated to evolutionarily divergent species.
journal_name
Dev Comp Immunoljournal_title
Developmental and comparative immunologyauthors
Wong C,Darby JM,Murphy PR,Pinfold TL,Lennard PR,Woods GM,Lyons AB,Flies ASdoi
10.1016/j.dci.2020.103882subject
Has Abstractpub_date
2021-02-01 00:00:00pages
103882eissn
0145-305Xissn
1879-0089pii
S0145-305X(20)30437-7journal_volume
115pub_type
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