Kate Hockemeyer: Stress response regulator HSF1 modulates NK cell anti-tumour immunity
Kate Hockemeyer shared on X:
“Excited to see our story showing that the stress response regulator HSF1 modulates NK cell anti-tumour immunity out in Nature Cell Biology. Thanks to fantastic work with Nikos Kourtis, Iannis Aifantis and team.
We examined HSF1 activity in the tumor immune micro environment and found it was lowest in NK cells relative to other populations but found variability in HSF1 activation leading us to make a mouse model of HSF1 overactivation.
We found that NK cells with HSF1 activation exhibit impaired cytotoxicity and IFNγ production leading to diminished NK cell-mediated anti-tumor immunity and accelerated tumor growth.
We found that both murine and patient melanoma tumors have a population of NK cells with high HSF1 activity and reduced expression of genes mediatingNK cell function, including IL2RB and IRF8
Finally, we show that HSF1 has direct binding and leads to upregulated expression of IL2RB and IRF8 suggesting that cellular stress and subsequent HSF1 activation lead to decreased NK cell effector function. Grateful to all coauthors and members of Aifantis Lab.”
Authors: Kathryn Hockemeyer, Theodore Sakellaropoulos, Xufeng Chen, Olha Ivashkiv, Maria Sirenko, Hua Zhou, Giovanni Gambi, Elena Battistello, Kleopatra Avrampou, Zhengxi Sun, Maria Guillamot, Luis Chiriboga, George Jour, Igor Dolgalev, Kate Corrigan, Kamala Bhatt, Iman Osman, Aristotelis Tsirigos, Nikos Kourtis and Iannis Aifantis
Source: Kate Hockemeyer/X
Kate Hockemeyer, MD, PhD, is affiliated with NYU School of Medicine, where she workes under the mentorship of Iannis Aifantis to investigate the role of the proteotoxic stress response in the melanoma tumor immune microenvironment. She completed the Transitional Year program at Memorial Sloan Kettering before beginning her Radiation Oncology Residency. Her research focuses on studying cancer cell-immune interactions in the context of radiation therapy for metastatic disease.
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