ORIGINAL RESEARCH article
Front. Immunol.
Sec. T Cell Biology
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1596802
Focal adhesion kinase plays an essential role in Th17 cell differentiation by stimulating NF-B signaling
Provisionally accepted
- 1Sogang University, Seoul, Republic of Korea
- 2Institute for Basic Science (IBS), Daejeon, Daejeon, Republic of Korea
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T helper type 17 (Th17) cells play critical roles in the pathogenesis of various autoimmune and inflammatory diseases; however, signaling pathways that affect Th17 cell differentiation are not fully understood. Here, we investigated whether focal adhesion kinase (FAK), an integrator of extracellular signals, regulates differentiation of Th17 cells. The findings reveal that Fak deficiency in CD4 T cells significantly reduces Th17 differentiation, while also promoting regulatory T (Treg) cell differentiation, thereby ameliorating symptoms of experimental autoimmune encephalomyelitis (EAE). Mechanistically, Fak deficiency inhibited nuclear translocation of the NF-B subunit RelA, thereby reducing the binding of RelA to the promoter region of Il17a. Moreover, pharmacological inhibition of FAK with the specific inhibitor PND1186 prevented Th17 differentiation in vitro, and reduced EAE symptoms in vivo. Thus, FAK plays an essential role in Th17 cell differentiation by stimulating NF- B signaling.
Keywords: FAK, Th17, NF-κB, T helper differentiation, EAE
Received: 20 Mar 2025; Accepted: 02 Sep 2025.
Copyright: © 2025 Kim, Lee, Sohn, Lee, Kim, Lee and Lee. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Gap Ryol Lee, Sogang University, Seoul, Republic of Korea
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