A tyrosine sulfation-dependent HLA-I modification identifies memory B cells and plasma cells.
Justin Tze Ho ChanYanling LiuSrijit KhanJonathan R St-GermainChunxia ZouLeslie Y T LeungJudi YangMengyao ShiEyal GrunebaumPaolo CampisiEvan J PropstTheresa HollerAmit Bar-OrJoan E WitherChristopher W CairoMichael F MoranAlexander F PalazzoMax D CooperGötz R A EhrhardtPublished in: Science advances (2018)
Memory B cells and plasma cells are antigen-experienced cells tasked with the maintenance of humoral protection. Despite these prominent functions, definitive cell surface markers have not been identified for these cells. We report here the isolation and characterization of the monoclonal variable lymphocyte receptor B (VLRB) N8 antibody from the evolutionarily distant sea lamprey that specifically recognizes memory B cells and plasma cells in humans. Unexpectedly, we determined that VLRB N8 recognizes the human leukocyte antigen-I (HLA-I) antigen in a tyrosine sulfation-dependent manner. Furthermore, we observed increased binding of VLRB N8 to memory B cells in individuals with autoimmune disorders multiple sclerosis and systemic lupus erythematosus. Our study indicates that lamprey VLR antibodies uniquely recognize a memory B cell- and plasma cell-specific posttranslational modification of HLA-I, the expression of which is up-regulated during B cell activation.
Keyphrases
- induced apoptosis
- multiple sclerosis
- cell cycle arrest
- systemic lupus erythematosus
- working memory
- endothelial cells
- endoplasmic reticulum stress
- signaling pathway
- rheumatoid arthritis
- poor prognosis
- oxidative stress
- single cell
- cell surface
- cell death
- transcription factor
- gene expression
- radiation therapy
- dna methylation
- disease activity
- long non coding rna
- genome wide
- drug induced