The balance between conventional and unconventional T follicular helper cells influences autoreactive B cell responses.

Invariant natural killer T (iNKT) cells are activated by glycolipids presented on CD1d. When iNKT cells interact with and activate B cells, they can differentiate into iNKT follicular helper (iNKTfh) cells, and here, we investigate how this, in turn, regulates conventional T follicular helper (Tfh)...

Full description

Bibliographic Details
Authors: He, Chenfei, Wang, Shan, Moreews, Marion, Pei, Shengduo, Chen, Guangchun, Li, Quan-Zhen, Del Monte Monge, Alberto, Ramiro, Almudena R, Cai, Curtis, Gaya, Mauro, Barral, Patricia, Buggert, Marcus, Batista, Facundo D, Karlsson, Mikael C I
Format: article
Publication Date:2025
Country:España
Institution:Instituto de Salud Carlos III (ISCIII)
Repository:Repisalud
Language:English
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/27058
Online Access:https://hdl.handle.net/20.500.12105/27058
Access Level:Open access
Keyword:CD1d
CP: Immunology
T follicular helper cells
apoptotic cells
autoimmune disease
germinal center
Description
Summary:Invariant natural killer T (iNKT) cells are activated by glycolipids presented on CD1d. When iNKT cells interact with and activate B cells, they can differentiate into iNKT follicular helper (iNKTfh) cells, and here, we investigate how this, in turn, regulates conventional T follicular helper (Tfh) cells. This is done in an autoimmune model where antibodies are produced against self-antigens relevant to the autoimmune disease systemic lupus erythematosus (SLE). We find a balance between iNKTfh and Tfh cells that directs the B cell response and influences Tfh cell generation. This altered balance also affects the specificities and increases the autoantibody response. We also show that CD1d expression by B cells is essential for iNKTfh cell generation. In conclusion, our data shed light on how T cell help for B cells is divided between conventional and unconventional helper cell populations and how this has an impact on autoreactive B cell responses.