aberrant expression of HLA Class‐I antigens in burkitt lymphoma cells
HLA class‐1 expression has been investigated by biochemical methods in 14 Burkitt lymphoma (BL) cell lines and the corresponding Epstein‐Barr virus (EBV)‐transformed lymphoblastoid cell lines (LCL) derived from the same individuals. Selective down‐regulation of one or more HLA class‐1 specificities...
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Veröffentlicht in: | International journal of cancer 1991-02, Vol.47 (4), p.544-550 |
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Zusammenfassung: | HLA class‐1 expression has been investigated by biochemical methods in 14 Burkitt lymphoma (BL) cell lines and the corresponding Epstein‐Barr virus (EBV)‐transformed lymphoblastoid cell lines (LCL) derived from the same individuals. Selective down‐regulation of one or more HLA class‐1 specificities was demonstrated in 9 out of 14 BL lines. The defect was restricted to a single HLA‐A allele in 3 of the lines (BL29, BL72, WW‐1‐BL). Four lines (BL28, BL37, BL41 and Jijoye M13) showed down‐regulation of both HLA‐A and ‐C alleles, and one (BL36) failed to express one HLA‐C allele. Only one BL line (WW‐2‐BL) had lost one HLA‐A and one HLA‐B allele. The allele‐specific defects were mainly detected in cell lines that had maintained the phenotypic characteristics of the original tumor. Expression of B‐cell activation markers and the EBV‐encoded nuclear antigen (EBNA)‐2 correlated with up‐regulation of the Cw4 allele in the P79 subline of the BL line Jijoye. Treatment with gamma‐interferon (IFN) resulted in full or partial reversion of the HLA class‐1 defects in some of the cases but had no significant effect in others. This was not due to a cell‐line‐related unresponsiveness to IFN, nor did it reflect an allele‐specific mode of regulation because the same allele could respond differently in different cell lines. The data suggest that defective expression of HLA class‐1 antigens, which appears to be more prevalent for alleles within the HLA‐A and ‐C loci, is a common feature of BL cell lines. Different regulatory mechanisms appear to be involved. |
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ISSN: | 0020-7136 1097-0215 |
DOI: | 10.1002/ijc.2910470412 |