AID in non-Hodgkin B-cell lymphomas: The consequences of on- and off-target activity.
Adv Immunol
; 161: 127-164, 2024.
Article
de En
| MEDLINE
| ID: mdl-38763700
ABSTRACT
Activation induced cytidine deaminase (AID) is a key element of the adaptive immune system, required for immunoglobulin isotype switching and affinity maturation of B-cells as they undergo the germinal center (GC) reaction in peripheral lymphoid tissue. The inherent DNA damaging activity of this enzyme can also have off-target effects in B-cells, producing lymphomagenic chromosomal translocations that are characteristic features of various classes of non-Hodgkin B-cell lymphoma (B-NHL), and generating oncogenic mutations, so-called aberrant somatic hypermutation (aSHM). Additionally, AID has been found to affect gene expression through demethylation as well as altered interactions between gene regulatory elements. These changes have been most thoroughly studied in B-NHL arising from GC B-cells. Here, we describe the most common classes of GC-derived B-NHL and explore the consequences of on- and off-target AID activity in B and plasma cell neoplasms. The relationships between AID expression, including effects of infection and other exposures/agents, mutagenic activity and lymphoma biology are also discussed.
Mots clés
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Lymphocytes B
/
Lymphome B
/
Centre germinatif
/
Cytidine deaminase
Limites:
Animals
/
Humans
Langue:
En
Journal:
Adv Immunol
Année:
2024
Type de document:
Article
Pays de publication:
États-Unis d'Amérique