GLOSSARY

N

• Neoantigen #

  A class of novel antigens that arise in cancer, but not normal cells. They are the result of mutations, mRNA variations, and/or aberrant translation, leading to expression of novel polypeptides, or are produced by oncogenic viruses integrated into the genome. If processed and presented on MHC molecules in tumor cells or picked up and presented on antigen presenting cells, neoantigens can promote antitumor immune responses.

• neoORF #

  A term referring to novel (neo) open reading frames in a gene transcript. NeoORFs may be created by frameshift mutations due to out-of-frame insertions or deletions (fs-indels) or gene fusions that have occurred in the gene that result in a novel polypeptide sequence. Alternative splicing events in a primary transcript of the wild-type gene(s) can also generate neoORFs. Expression of neoORFs in patients with cancer has been found to elicit antitumor immune responses and has been associated with clinical benefit from immunotherapy, suggesting diagnostic and potential therapeutic value in cancer therapy. The translation of a neoORF may depend on whether the RNA escapes from the nonsense-mediated decay pathway.

• netMHCIIpan #

  A bioinformatic tool that predicts peptide binding to MHC-II molecules. It uses artificial neural networks trained on binding affinity and eluted ligand data from human MHC class-II isotypes HLA-DR, HLA-DQ, HLA-DP, and mouse H-2-IA or H2-IE. Predictions can be made for any MHC class-II of known sequence and peptides of any length, and, based on extrapolation from MHC structural information, can be used for MHC alleles for which no binding or eluted ligand data has been collected. netMHCIIpan is supported by Technical University of Denmark (DTU).

• netMHCpan #

  A bioinformatic tool that predicts peptide binding to MHC molecules. It uses artificial neural networks trained on binding affinity and eluted ligand data from humans, mice, cattle, primates, swine, equines, and dogs. Predictions for binding to MHC-I molecules in the netMHCpan database can be made for peptides of any length, and, based on extrapolation from MHC structural information, can be used for MHC alleles for which no binding or eluted ligand data has been collected. Predictions for binding to uploaded custom MHC-I molecules can also be made. netMHCpan is supported by the Technical University of Denmark (DTU).

• NKG2D (CD314) #

  Alternative names: KLRK1

  In humans and in mice, NKG2D can be found on the surface of: T cells, B cells, NK cells, macrophages/monocytes, granulocytes

  Ligands: MICA, MICB, ULBP2, ULBP1, H60 (mice)

  Associated molecules: DAP10 dimer or DAP10 and DAP12 (in mice)

  Function: MHC-1 HLA-E molecule recognition, NK cell activation

  Additional information: NKG2D is also known as CD314. CD314 is a key activating receptor on NK cells. CD314 is also a costimulatory molecule on T cells and promotes the development of memory CD8⁺ T cells. CD314 expression on the surface of B cells plays a key role in B cell proliferation and differentiation and the regulation of IgE production. Ligands of CD314 are homologous to MHC class I molecules, and come from the MIC or RAET1/ULBP family. The expression of NKG2D ligands is induced during cellular stress (e.g., infection, senescence) or genomic stress (e.g., mutations, increased proliferation, viral replication).

• NKp46 (CD335) #

  Alternative names: Ly-94, NCR1

  In humans and in mice, NKp46 can be found on the surface of: NK cells

  Ligands: Viral glycoproteins (hemagglutinins), Heparan sulfate proteoglycans

  Associated molecules: CD3ζ and FcεRIγ

  Function: NK cell cytotoxicity, NK cell activation

  Additional information: NKp46 is also known as CD335. CD335 is part of the natural cytotoxicity receptor (NCR) family. CD335 plays a role in antitumor and antiviral immunity, conferring tumor cell recognition and binding of viral hemagglutinins. Engagement of CD335 on NK cells results in increased cytokine production and cytotoxicity. CD335 is expressed on the surface of activated and resting NK cells.