Bob1 maintains T follicular helper cells for long-term humoral immunity.
Masahiro YanagiIppei IkegamiRyuta KamekuraTatsuya SatoTaiki SatoShiori KamiyaKosuke MurayamaSumito JitsukawaFumie ItoAkira YorozuMiho KiharaTakaya AbeHiromi TakakiKoji KawataKatsunori ShigeharaSatsuki MiyajimaHirotaka NishikioriAkinori SatoNoritsugu TohseKen-Ichi TakanoHirofumi ChibaShingo IchimiyaPublished in: Communications biology (2024)
Humoral immunity is vital for host protection, yet aberrant antibody responses can trigger harmful inflammation and immune-related disorders. T follicular helper (Tfh) cells, central to humoral immunity, have garnered significant attention for unraveling immune mechanisms. This study shows the role of B-cell Oct-binding protein 1 (Bob1), a transcriptional coactivator, in Tfh cell regulation. Our investigation, utilizing conditional Bob1-deficient mice, suggests that Bob1 plays a critical role in modulating inducible T-cell costimulator expression and cellular respiration in Tfh cells. This regulation maintains the long-term functionality of Tfh cells, enabling their reactivation from central memory T cells to produce antibodies during recall responses. In a bronchial asthma model induced by house dust mite (HDM) inhalation, Bob1 is observed to enhance HDM-specific antibodies, including IgE, highlighting its pivotal function in Tfh cell regulation. Further exploration of Bob1-dependent mechanisms in Tfh cells holds promise for governing protective immunity and addressing immune-related disorders.
Keyphrases
- induced apoptosis
- cell cycle arrest
- immune response
- signaling pathway
- oxidative stress
- cell death
- gene expression
- working memory
- poor prognosis
- chronic obstructive pulmonary disease
- bone marrow
- cystic fibrosis
- optical coherence tomography
- lung function
- allergic rhinitis
- health risk
- deep learning
- long non coding rna
- heat shock protein