Table 1.
Factors may contribute to the defects in immune recognition of BL cells.
| Factor | Cells Affected | Function(s)/defect(s) in Immune Evasion |
|---|---|---|
| EBNA1 | >90% eBL | Negative regulation of own mRNA translation [64] |
| 5–10% sBL | Internal gly-ala repeat blocks proteasomal degradation and consequent | |
| 40% HIV associated BL | HLA class I presentation [63] | |
|
| ||
| C-myc | All BL | Downregulation of HLA class I [30] |
| Antagonism of NF-κB pathway | ||
| Negative regulation of STAT1 signaling | ||
| Impairment of interferon response [59] | ||
| Downregulation of accessory molecules important in immune response: LFA-1, LFA-3, ICAM-1, and TAP [86–90] | ||
|
| ||
| HLA class I | All BL | Down-regulated in BL [71–74] |
| Downregulation of CD80/86 in BL decreases HLA class I signaling | ||
|
| ||
| HLA class II | All BL | Downregulation of CD80/86 in BL decreases HLA class II signaling |
| Upregulation of HLA-DO causes decrease in formation of class | ||
| II/peptide complexes [91, 92] BLAIM may impair functional Ag | ||
| presentation by HLA class II (unpublished data). | ||