US 12,234,480 B2
Therapeutic methods involving modulating inflammasome activation of myeloid-derived suppressor cells
Bruce R. Blazar, Golden Valley, MN (US); Brent Koehn, Elk River, MN (US); Peter J. Murray, Memphis, TN (US); Jenny P. Y. Ting, Chapel Hill, NC (US); Robert Zeiser, Freiburg (DE); and Jeff S. Miller, Little Canada, MN (US)
Assigned to Regents of the University of Minnesota, Minneapolis, MN (US); The University of North Carolina at Chapel Hill, Chapel Hill, NC (US); Albert-Ludwigs-Universität Freiburg, Freiburg (DE); and St. Jude Children's Research Hospital, Inc., Memphis, TN (US)
Filed by Regents of the University of Minnesota, Minneapolis, MN (US); The University of North Carolina at Chapel Hill, Chapel Hill, NC (US); Albert-Ludwig Universitat Freiburg, Freiburg (DE); and St. Jude Children's Research Hospital, Inc., Memphis, TN (US)
Filed on Dec. 11, 2020, as Appl. No. 17/119,832.
Application 17/119,832 is a continuation of application No. 15/747,902, granted, now 10,894,061, previously published as PCT/US2016/045739, filed on Aug. 5, 2016.
Claims priority of provisional application 62/201,990, filed on Aug. 6, 2015.
Prior Publication US 2021/0128612 A1, May 6, 2021
This patent is subject to a terminal disclaimer.
Int. Cl. C12N 5/0787 (2010.01); A61K 35/12 (2015.01); A61K 39/00 (2006.01); A61K 45/06 (2006.01); A61P 37/06 (2006.01); C12N 5/078 (2010.01); C12N 5/0786 (2010.01)
CPC C12N 5/0642 (2013.01) [A61K 39/001 (2013.01); A61K 39/461 (2023.05); A61K 39/4611 (2023.05); A61K 39/4621 (2023.05); A61K 39/46434 (2023.05); A61K 45/06 (2013.01); A61P 37/06 (2018.01); C12N 5/0634 (2013.01); C12N 5/0645 (2013.01); C12N 5/0648 (2013.01); A61K 2035/122 (2013.01); A61K 2035/124 (2013.01); A61K 2039/515 (2013.01); A61K 2039/545 (2013.01); A61K 2039/577 (2013.01); C12N 2501/22 (2013.01); C12N 2501/2313 (2013.01); C12N 2501/24 (2013.01)] 8 Claims
 
1. A human myeloid-derived suppressor cell (MDSC) deficient in apoptosis-associated speck-like protein containing a CARD (ASC), wherein the MDSC comprises:
i) a genetic modification of the ASC gene resulting in ASC deficiency, or
ii) a genetic knockdown of ASC via shRNA targeting the ASC gene or siRNA targeting the ASC gene.