Method for optimizing t cells for immuno-therapy
AssigneeCeMM - Forschungszentrum für Molekulare Medizin GmbH
InventorsPaul DATLINGER, Evgeniia PANKEVICH, Christoph BOCK
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AssigneeCeMM - Forschungszentrum für Molekulare Medizin GmbH
InventorsPaul DATLINGER, Evgeniia PANKEVICH, Christoph BOCK
Estimating the term…
The present invention is in the field of immunotherapy, in particular cell-based immunotherapies, e.g. for the treatment of cancer. Specifically, the present invention concerns the depletion or inactivation of RHOG and/or the suppression of RHOG expression and/or activity in T cells (in particular human T cells), e.g., CAR T cells, in vitro and/or in vivo. Therefore, the present invention provides RHOG modulators which are suitable for suppressing, impairing or abolishing the expression and/or activity of RHOG in a mammalian N cell such as a T cell. Moreover, the present invention relates to medical uses of such a RHOG modulator or T cells (e.g. CAR T cells) which comprise such a RHOG modulator or which have been contacted with such a RHOG modulator, e.g. for the treatment of cancer, as well as uses of such a RHOG modulator for culturing and/or producing T cells inviro, e.g., for adoptive cell transfer. Combinations of a RHOG modulator according to the invention and synthetic antigen receptors such as CARs are also encompassed by the present invention. Furthermore, the present invention provides specific CRISPR gRNAs and specific combinations of CRISPR gRNAs and CRISPR modifiers.
A method of preventing, ameliorating, or treating a disease or disorder, said method comprising administering an effective amount of a T cell or a population thereof to a subject in need thereof, wherein said T cell comprises
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An engineered mammalian cell or a population thereof, said engineered mammalian cell comprising the following (I) and (II):
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A pharmaceutical composition comprising a T cell or a population thereof, wherein said T cell comprises
A CAR T cell population in which expression of RHOG, HAVCR2, VAMP4, SLC35B3, TRAF1, NOTCH2, PHF8, DUSP6, DAW1, ZNF16, TCF4, PRSS3, LACTB, TMTC3, CD300LB, MORC3 and/or CDKN2A is suppressed.
Dependencies are inferred from the claim text.