Research Summary
Programmed cell death–cell suicide–is a fundamental biological process. We now understand that cells can kill themselves in several different ways, and that how a cell dies is a key determinant of the immune response generated by that dying cell. The Oberst lab studies how inflammatory forms of cell suicide occur, and how they affect the immune response to pathogens, cancer cells, and auto-antigens.
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Publications
The following publications were retrieved from PubMed:
De novo necroptosis creates an inflammatory environment mediating tumor susceptibility to immune checkpoint inhibitors.
Workenhe ST, Nguyen A, Bakhshinyan D, Wei J, Hare DN, MacNeill KL, Wan Y, Oberst A, Bramson JL, Nasir JA, Vito A, El-Sayes N, Singh SK, McArthur AG, Mossman KL.
Commun Biol. 2020 Nov 4; 1(3)645
Identification of MYC as an antinecroptotic protein that stifles RIPK1-RIPK3 complex formation.
Seong D, Jeong M, Seo J, Lee JY, Hwang CH, Shin HC, Shin JY, Nam YW, Jo JY, Lee H, Kim HJ, Kim HR, Oh JH, Ha SJ, Kim SJ, Roe JS, Kim W, Cheong JW, Bae KH, Lee SC, Oberst A, Vandenabeele P, Shin DH, Lee EW, Song J.
Proc Natl Acad Sci U S A. 2020 Aug 18; 33(117)19982-19993
T cells instruct myeloid cells to produce inflammasome-independent IL-1β and cause autoimmunity.
Jain A, Irizarry-Caro RA, McDaniel MM, Chawla AS, Carroll KR, Overcast GR, Philip NH, Oberst A, Chervonsky AV, Katz JD, Pasare C.
Nat Immunol. 2020 Jan; 1(21)65-74