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 language | English (US) |
|---|---|
| Article number | 108796 |
| Journal | Biomedicine and Pharmacotherapy |
| Volume | 114 |
| DOIs | |
| State | Published - Jun 1 2019 |
| Externally published | Yes |
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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 journal › Article
}
TY - JOUR
T1 - BAFF promotes T cell activation through the BAFF-BAFF-R-PI3K-Akt signaling pathway
AU - Hu, Shanshan
AU - Wang, Rui
AU - Zhang, Mei
AU - Liu, Kangkang
AU - Tao, Juan
AU - Tai, Yu
AU - Zhou, Weijie
AU - Wang, Qingtong
AU - Wei, Wei
PY - 2019/6/1
Y1 - 2019/6/1
N2 - 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.
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.
KW - B-cell activating factor from the tumor necrosis factor family (BAFF)
KW - B-cell activating factor from the tumor necrosis factor family receptor (BAFF-R)
KW - Phosphoinositide 3-kinase (PI3K)
KW - T cell activation
KW - Transmembrane activator and CAML interactor (TACI)
UR - http://www.scopus.com/inward/record.url?scp=85063346029&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85063346029&partnerID=8YFLogxK
U2 - 10.1016/j.biopha.2019.108796
DO - 10.1016/j.biopha.2019.108796
M3 - Article
C2 - 30921706
AN - SCOPUS:85063346029
VL - 114
JO - Biomedicine and Pharmacotherapy
JF - Biomedicine and Pharmacotherapy
SN - 0753-3322
M1 - 108796
ER -