Philip Lab
@philiplabvandy
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Working together at the frontier of cancer and immunology to advance cancer care, science, and education
Joined August 2019
And a big thank you and shout out to @EricSkaar @kh_oliver @VI4Research @bwfund for creating and supporting this great program to bring scientists and artists together!.
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We also got to work with senior Kya Knight @fisk1866 who painted this piece showing T cells attacking cancer cells
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Check out VUMC reporter piece on @jjroetman @CIR_AACR paper featuring amazing artwork by senior Halle Borowski @williamandmary created during the @ArtLab_Vandy @VI4Research Summer 2023 program!.
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We welcome feedback and suggestions, and a big thank you to our colleagues.@VUMC_VCI @VUMC_Cancer @VUMCDIsoveries @Vandy_Biomed.for all their support! 7/7.
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We hypothesize that peptide/MHC-TCR affinity may play a role in the divergent antigen-dependent differentiation we observed as self-shared antigens are usually lower affinity. 6/7.
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Though self/shared-reactive T cells were PD1- and TCF1+, they were as dysfunctional as tumor-specific T cells and failed to regain effector function with ICB therapy. 5/7
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We found that tumor-specific T cells entered the classic PD1+ TCF1- dysfunctional state in tumors, while self/shared-reactive T cells only persisted in the spleen in a PD1- TCF1+ state. 4/7
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Immune checkpoint blockade (ICB) therapies can unleash T cell responses against tumors but can also cause unwanted toxicity, or immune-related adverse events (irAE), when T cells attack self/shared antigens in non-cancerous tissues. 3/7.
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@jjroetman developed a unique cancer model in which we could study CD8 T cell responses against tumor-specific antigens and self/shared antigens. 2/7.
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Happy to present our latest paper in @CIR_AACR from @jjroetman, the whole @philiplabvandy team and Drs. Youngmin Lee and Ting-Fang Less @VUMCSurgery !.
#OnlineFirst: Tumor-reactive CD8+ #Tcells enter a TCF1+PD1– dysfunctional state, by @jjroetman, Mary Philip et al. @immuno_minna @VUmedicine
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Immune checkpoint blockade (ICB) can unleash T cell responses against tumors but can also cause unwanted toxicity, or immune-related adverse events (irAE), when T cells attack self/shared antigens in non-cancerous tissues. 3/7.
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@jjroetman developed a unique cancer model in which we could study CD8 T cell responses against tumor-specific antigens and self/shared antigens. 2/7.
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Congratulations Endeavor team at Vanderbilt, University of Tennessee, University of Pennsylvania: Jeffrey Rathmell, Alyssa Hasty, Liza Makowski, Kathryn Wellen @jeffrathmell @hasty4 @MakowskiLab @WellenLab @vumc_cancer @PennMedicine
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Congratulations Andrea!.
Congratulations to Dr. Andrea Schietinger, who received the AACR-Irving Weinstein Foundation Distinguished Lectureship. #Immunology
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Last and most important, a big shoutout to all our amazing colleagues @VUMC_VCI @VUMC_Cancer @VUMCDIsoveries @Vandy_Biomed especially @JeffRathmell @SchietingerLab for all their support! 7/7.
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By dissecting the earliest epigenetic and gene expression programs that mediate dysfunction, we can design new strategies to prevent T cell dysfunction in patients with cancer. 6/7.
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We think that cancers induce rapid T cell dysfunction because they (i) fail to provide T cells with inflammation-associated signaling necessary to induce functional differentiation and (ii) impose negative regulatory signals that shut down T cell function. 5/7.
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