allogeneic TCRa/b-depleted HA-1 minor histocompatibility antigen-reactive TCR-modified RQR8-expressing T cells BSB-1001
Term · Oncology and biomedicine · MLC-T-ONC-009947
A preparation of T-cell receptor (TCR) alpha and beta (TCRa/b)-depleted donor-derived T lymphocytes that have been transduced with a lentivirus vector encoding a TCR specific for HLA-A*02:01-restricted minor histocompatibility antigen HA-1 (HA1) and expressing RQR8, with potential immunomodulating and antineoplastic activities. Following HLA-matched allogeneic hematopoietic cell transplantation (HCT) in HLA-A*02:01 positive patients, allogeneic TCRa/b-depleted HA-1 minor histocompatibility antigen-reactive TCR-modified RQR8-expressing T cells BSB-1001 specifically recognize and bind to HA-1 expressed on tumor cells. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing HLA-A*02:01 HA-1. HA-1 is a lineage-specific antigen found on leukemia cells. BSB-1001 carries the universal RQR8 safety "off" switch, which allows selective removal of the T-cells through both complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) following administration of rituximab if unacceptable side-effects occur. CRISPR-cas9 editing of the donor T cells deletes the endogenous TCRa/b chains. Depletion of TCRa/b increases expression of the transduced TCR and reduces risk of graft-versus-host disease (GVHD) caused by native TCRs.
| Identifier | MLC-T-ONC-009947 |
|---|---|
| Field | Oncology and biomedicine |
| Synonyms | allogeneic anti-HA-1 T cells BSB-1001; allogeneic anti-HA-1 TCR-engineered T cells BSB-1001; allogeneic anti-miHA-1 TCR lentivector transduced T cells BSB-1001; allogeneic HA-1-targeting TCR T cells BSB-1001; allogeneic miHA-reactive TCR-modified T cells BSB-1001; T-cell receptor engineered donor T cells BSB-1001 |
| References | National Cancer Institute Thesaurus (CC BY 4.0) |
Record as JSON
{
"id": "MLC-T-ONC-009947",
"term": "allogeneic TCRa/b-depleted HA-1 minor histocompatibility antigen-reactive TCR-modified RQR8-expressing T cells BSB-1001",
"field": "Oncology and biomedicine",
"definition": "A preparation of T-cell receptor (TCR) alpha and beta (TCRa/b)-depleted donor-derived T lymphocytes that have been transduced with a lentivirus vector encoding a TCR specific for HLA-A*02:01-restricted minor histocompatibility antigen HA-1 (HA1) and expressing RQR8, with potential immunomodulating and antineoplastic activities. Following HLA-matched allogeneic hematopoietic cell transplantation (HCT) in HLA-A*02:01 positive patients, allogeneic TCRa/b-depleted HA-1 minor histocompatibility antigen-reactive TCR-modified RQR8-expressing T cells BSB-1001 specifically recognize and bind to HA-1 expressed on tumor cells. This may lead to cytotoxic T-lymphocyte (CTL)-mediated elimination of tumor cells expressing HLA-A*02:01 HA-1. HA-1 is a lineage-specific antigen found on leukemia cells. BSB-1001 carries the universal RQR8 safety \"off\" switch, which allows selective removal of the T-cells through both complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) following administration of rituximab if unacceptable side-effects occur. CRISPR-cas9 editing of the donor T cells deletes the endogenous TCRa/b chains. Depletion of TCRa/b increases expression of the transduced TCR and reduces risk of graft-versus-host disease (GVHD) caused by native TCRs.",
"synonyms": [
"allogeneic anti-HA-1 T cells BSB-1001",
"allogeneic anti-HA-1 TCR-engineered T cells BSB-1001",
"allogeneic anti-miHA-1 TCR lentivector transduced T cells BSB-1001",
"allogeneic HA-1-targeting TCR T cells BSB-1001",
"allogeneic miHA-reactive TCR-modified T cells BSB-1001",
"T-cell receptor engineered donor T cells BSB-1001"
],
"references": [
"National Cancer Institute Thesaurus"
],
"url": "https://mlchart.com/terminology/oncology/allogeneic-tcra-b-depleted-ha-1-minor-histocompatibility-antigen-reactive-tcr-t/"
}
Record 834 of 17,721 in Oncology and biomedicine terminology (MLC-0111). Request the full dataset.