Publication: CD39 is an antibody-secreting B-cell marker that modulates germinal center and antibody responses during infection

Publié dans:

Auteurs: Laura Almada, Yamila N Gazzoni, Cristian G Beccaria, Facundo Fiocca Vernengo, Santiago Boccardo, Melisa Gorosito Serrán, Apurwa Trivedi, Carola G Vinuesa, Simon C Robson, Eva V Acosta Rodríguez, Mauro Gaya, Carolina L Montes, Adriana Gruppi

Résumé

CD39 is an ectoenzyme in immune cells that regulates purinergic signaling by converting extracellular ATP into adenosine (ADO). Although first described on EBV-transformed B cells, CD39’s role in humoral immunity remains unclear. Using murine infection models and human samples, we confirm and extend previous findings showing that high CD39 expression identifies antibody-secreting cells (ASC) across differentiation stages, including ASC derived from memory B cells, and in various tissues, regardless of the infection phase. CD39 was resistant to enzymatic digestion, facilitating ASC identification in processed tissues. We found that while CD39 was not essential for B-cell differentiation into ASC, it remained functionally active as an ectoenzyme. ASC as well as germinal center (GC) B cells expressed ADO receptors, making them responsive to ADO signaling. Consistently, systemic ADO administration impaired GC reactions without altering the ASC number in infected mice. However, in vitro , ADO reduces antibody production both in ASC and in B cells undergoing differentiation and also impairs the differentiation of activated B cells. Finally, B cell–specific CD39 deficiency increased GC B-cell frequencies in infected mice, likely due to reduced ADO levels. These findings highlight the relevance of the purinergic pathway in B-cell biology.

Lien vers HAL – amu-05515411

Lien vers le DOI – 10.3389/fimmu.2025.1547929