BAFF promotes T cell activation through the BAFF-BAFF-R-PI3K-Akt signaling pathway

Shanshan Hu, Rui Wang, Mei Zhang, Kangkang Liu, Juan Tao, Yu Tai, Weijie Zhou, Qingtong Wang, Wei Wei

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

B-cell activating factor from the tumor necrosis factor family (BAFF) has revealed its critical role in B cell proliferation and survival, as well as the pathogenesis of T-cell mediated autoimmune disease. However, the effect and molecular mechanisms of BAFF on T cell physiological function have not been fully elucidated. In this study it was seen that BAFF can promote the vitality of purified T cells, increase the proportion of CD3 + CD4 + , CD4 + CD25 + , CD4 + CD154 + , and CD4 + CD69 + subgroups and reduce the proportion of CD4 + CD62L + subgroups. Negating BAFF activity with Atacicept (TACI-Fc) reverses vitality and activation of T cells. Furthermore, immunofluorescence detection revealed that BAFF promotes the expression of BAFF receptor (BAFF-R) and transmembrane activator and CAML interactor (TACI) in T cells. Flow cytometry displayed that BAFF/BAFF-R activates the PI3K-Akt signaling pathway while the application of PI3K inhibitor (wortmannin) illuminated that BAFF induces T cell vitality and activation through the PI3K-Akt signaling pathway. We conclude that BAFF is involved in not only the physiology of B cells, but also that of T cells. BAFF affects physiological T-cell activation through BAFF-R-mediated activation of the PI3K-Akt signaling pathway which mirrors one of the pathological mechanisms of T cell-mediated autoimmune diseases.

Original languageEnglish (US)
Article number108796
JournalBiomedicine and Pharmacotherapy
Volume114
DOIs
StatePublished - Jun 1 2019
Externally publishedYes

Fingerprint

B-Cell Activation Factor Receptor
Phosphatidylinositol 3-Kinases
T-Lymphocytes
Autoimmune Diseases
B-Lymphocytes
B-Cell Activating Factor
Fluorescent Antibody Technique
Cell Survival
Flow Cytometry
Tumor Necrosis Factor-alpha

Keywords

  • B-cell activating factor from the tumor necrosis factor family (BAFF)
  • B-cell activating factor from the tumor necrosis factor family receptor (BAFF-R)
  • Phosphoinositide 3-kinase (PI3K)
  • T cell activation
  • Transmembrane activator and CAML interactor (TACI)

ASJC Scopus subject areas

  • Pharmacology

Cite this

BAFF promotes T cell activation through the BAFF-BAFF-R-PI3K-Akt signaling pathway. / Hu, Shanshan; Wang, Rui; Zhang, Mei; Liu, Kangkang; Tao, Juan; Tai, Yu; Zhou, Weijie; Wang, Qingtong; Wei, Wei.

In: Biomedicine and Pharmacotherapy, Vol. 114, 108796, 01.06.2019.

Research output: Contribution to journalArticle

Hu, S, Wang, R, Zhang, M, Liu, K, Tao, J, Tai, Y, Zhou, W, Wang, Q & Wei, W 2019, 'BAFF promotes T cell activation through the BAFF-BAFF-R-PI3K-Akt signaling pathway', Biomedicine and Pharmacotherapy, vol. 114, 108796. https://doi.org/10.1016/j.biopha.2019.108796
Hu, Shanshan ; Wang, Rui ; Zhang, Mei ; Liu, Kangkang ; Tao, Juan ; Tai, Yu ; Zhou, Weijie ; Wang, Qingtong ; Wei, Wei. / BAFF promotes T cell activation through the BAFF-BAFF-R-PI3K-Akt signaling pathway. In: Biomedicine and Pharmacotherapy. 2019 ; Vol. 114.
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AU - Tao, Juan

AU - Tai, Yu

AU - Zhou, Weijie

AU - Wang, Qingtong

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AB - B-cell activating factor from the tumor necrosis factor family (BAFF) has revealed its critical role in B cell proliferation and survival, as well as the pathogenesis of T-cell mediated autoimmune disease. However, the effect and molecular mechanisms of BAFF on T cell physiological function have not been fully elucidated. In this study it was seen that BAFF can promote the vitality of purified T cells, increase the proportion of CD3 + CD4 + , CD4 + CD25 + , CD4 + CD154 + , and CD4 + CD69 + subgroups and reduce the proportion of CD4 + CD62L + subgroups. Negating BAFF activity with Atacicept (TACI-Fc) reverses vitality and activation of T cells. Furthermore, immunofluorescence detection revealed that BAFF promotes the expression of BAFF receptor (BAFF-R) and transmembrane activator and CAML interactor (TACI) in T cells. Flow cytometry displayed that BAFF/BAFF-R activates the PI3K-Akt signaling pathway while the application of PI3K inhibitor (wortmannin) illuminated that BAFF induces T cell vitality and activation through the PI3K-Akt signaling pathway. We conclude that BAFF is involved in not only the physiology of B cells, but also that of T cells. BAFF affects physiological T-cell activation through BAFF-R-mediated activation of the PI3K-Akt signaling pathway which mirrors one of the pathological mechanisms of T cell-mediated autoimmune diseases.

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