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US 2024/0207378 A1Published application
Beta-2 microglobulin-deficient cells
AssigneeUniversity of Washington through its Center for Commercialization
InventorsDavid W. Russell, Roli K. Hirata
Life of this patent
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Abstract
The invention provides isolated primate cells preferably human cells that comprise a genetically engineered disruption in a beta-2 microglobulin (B2M) gene, which results in deficiency in MHC class I expression and function. Also provided are the method of using the cells for transplantation and treating a disease condition.
Claims25
1-43. (canceled)
An isolated cell comprising
- a. a genetically engineered disruption of an endogenous β2 microglobulin (B2M) gene,
- b. one or more polynucleotides capable of encoding a single chain fusion non-classical human leukocyte antigen (HLA) class I protein, wherein the single chain fusion non-classical HLA class I protein comprises at least a portion of B2M covalently linked to at least a portion of a HLA-F class I α chain,
- wherein the single chain fusion classical HLA class I protein is capable of normal function with respect to engaging an inhibitory receptor on the surface of natural killer (NK) cells.
An isolated cell comprising
- a. a genetically engineered disruption of an endogenous β2 microglobulin (B2M) gene,
- b. one or more polynucleotides capable of encoding a single chain fusion non-classical human leukocyte antigen (HLA) class I protein, wherein the single chain fusion non-classical HLA class I protein comprises at least a portion of B2M covalently linked to at least a portion of a HLA-G class I α chain,
- wherein the single chain fusion classical HLA class I protein is capable of normal function with respect to engaging an inhibitory receptor on the surface of natural killer (NK) cells.
An isolated cell comprising
- a. a genetically engineered disruption of an endogenous β2 microglobulin (B2M) gene,
- b. one or more polynucleotides capable of encoding a single chain fusion non-classical human leukocyte antigen (HLA) class I protein, wherein the single chain fusion non-classical HLA class I protein comprises at least a portion of B2M covalently linked to at least a portion of a HLA-E class I α chain,
- wherein the single chain fusion classical HLA class I protein is capable of normal function with respect to engaging an inhibitory receptor on the surface of natural killer (NK) cells.
An isolated cell comprising
- a. a genetically engineered disruption of an endogenous β2 microglobulin (B2M) gene,
- b. one or more polynucleotides capable of encoding a single chain fusion human leukocyte antigen (HLA) class I protein, wherein the single chain fusion HLA class I protein comprises at least a portion of B2M covalently linked to at least a portion of a HLA-A class I α chain,
- wherein the single chain fusion classical HLA class I protein is capable of normal function with respect to engaging an inhibitory receptor on the surface of natural killer (NK) cells.
An isolated cell comprising
- a. a genetically engineered disruption of an endogenous β2 microglobulin (B2M) gene,
- b. one or more polynucleotides capable of encoding a single chain fusion human leukocyte antigen (HLA) class I protein, wherein the single chain fusion HLA class I protein comprises at least a portion of B2M covalently linked to at least a portion of a HLA-B class I α chain,
- wherein the single chain fusion classical HLA class I protein is capable of normal function with respect to engaging an inhibitory receptor on the surface of natural killer (NK) cells.
An isolated cell comprising
- a. a genetically engineered disruption of an endogenous β2 microglobulin (B2M) gene,
- b. one or more polynucleotides capable of encoding a single chain fusion human leukocyte antigen (HLA) class I protein, wherein the single chain fusion HLA class I protein comprises at least a portion of B2M covalently linked to at least a portion of a HLA-C class I α chain,
- wherein the single chain fusion classical HLA class I protein is capable of normal function with respect to engaging an inhibitory receptor on the surface of natural killer (NK) cells.
Dependencies are inferred from the claim text.