Highlights d Iterative KO screens reveal a new pathway controlling HLA-I antigen presentation d SPPL3 suppresses B3GNT5 activity affecting the cell surface GSL repertoire d B3GNT5-generated GSLs limit the capacity of HLA-I to interact with natural ligands d Inhibition of GSL synthesis in glioma enhances anti-tumor immune activation
In our article entitled ''The SPPL3-defined glycosphingolipid repertoire orchestrates HLA class I-mediated immune responses,'' we employed a glioblastoma cell line in some experiments to which we referred as U373. Short tandem repeat profiling-based authentication revealed that we had actually used the glioblastoma cell line U-251 instead of U373. The U-251 and U373 cell lines were derived from two different glioblastoma patients. An error occurring decades ago caused U-251 to be incorrectly distributed by multiple cell line repositories as ''U373,'' resulting in a misreporting of the cell line's name that still occasionally occurs today (https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC4303149/). We have now corrected the name of the cell line we used to U-251. The misidentification does not affect the results, conclusions and implications discussed. The authors apologize for any confusion that may have been caused.
A single model system for integrative studies on multiple facets of antigen presentation is lacking. PAKC is a novel panel of ten cell lines knocked out for individual components of the HLA class I antigen presentation pathway. PAKC will accelerate HLA‐I research in the fields of oncology, infectiology, and autoimmunity.
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