Apoptosis of Dendritic Cells and Autoimmune Disease

² Anhui Provincial Key Laboratory for Conservation and Exploitation of Biological Resources, College of Life Science, Anhui Normal University, 241000 Wuhu, Anhui, China

^*Correspondence: 19920012@wnmc.edu.cn (Haihua Wang); yuekang.xu@hotmail.com (Yuekang Xu)
^†These authors contributed equally.

Front. Biosci. (Landmark Ed) 2024, 29(4), 157; https://doi.org/10.31083/j.fbl2904157

Submitted: 17 October 2023 | Revised: 2 March 2024 | Accepted: 7 March 2024 | Published: 22 April 2024

This is an open access article under the CC BY 4.0 license.

Abstract

Dendritic cells (DCs), the most efficient antigen-presenting cells (APCs), bridge the innate and adaptive immune systems. As such, the turn-over of DCs is critical during autoimmune responses, and the dysregulation of DC apoptosis could cause severe immune destruction in the host. For example, reduction of immunogenic DCs by increased apoptosis could lead to immune tolerance to pathogen infection that might allow exposure of nuclear autoantigens, whereas reduced apoptosis could result in long-term lymphocyte activation to break the immune tolerance for the development of autoimmune disease. Thus, keeping a balance between survival and apoptosis of DCs is crucial to maintain immune homeostasis. In this review, we summarize the recent development on the factors inducing DC apoptosis and their underlying mechanisms to provide insights into the immunopathogenesis of some autoimmune diseases, which could lead to effective therapeutic interventions in the clinics.

Keywords

dendritic cells

apoptosis

autoimmune diseases

Funding

2022AH051243/Key Project of Natural Science Research of Anhui Provincial Education Department

2023AH051766/Key Project of Natural Science Research of Anhui Provincial Education Department

WK2022Z03/Key Project of Natural Science Research of Wannan Medical Research

WYRCQD2021001/Scientific Research Foundation for Doctor

WYRCQD2023008/Scientific Research Foundation for Doctor

S202310368036/Project of Anhui Province College Student Innovation and Entrepreneurship Training Program

Figures

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Fig. 1.

The regulation of DC apoptosis. DC apoptosis is regulated by (1) TNF superfamily molecules, such as TRANCE/RANK, TRAIL/DR4/5, CD40/CD40L and CD95(Fas)/FasL; (2) Bcl-2 family molecules including pro-apoptotic (Bax, Bak), anti-apoptotic (A1, Bcl-2, Bcl-w, Bcl-xl, Mcl-1) and BH3-only proteins (Bim, Bid, Puma, Noxa, Hrk, Bik, Bmf, Bad); (3) NLR family, for example, NLRC4; (4) miRNAs, such as miR-29b/c; (5) cytokines such as GM-CSF, leptin, IL-21/10, IFN-I and IFN- $\beta$ ; (6) other factors such as insulin-like growth factor I. DC, dendritic cells; TNF, tumor necrosis factor; BH, Bcl-2 homology; FADD, fas-associated protein with death domain; DR, death receptor; FLIP, FADD-like IL-1 $\beta$ -converting enzyme-inhibitory protein; GM-CSF, granulocyte-maccrophage colony-stimulating factor; JNK, Jun Nterminal kinase; LPS, lipopolysaccharide; PI3K, phosphatidylinositol 3-kinase; RANK, receptor activator of NF- $\kappa{}$ B; TLR, toll-like receptor; TRAIL, TNF-related apoptosis-inducing ligand; TRANCE, TNF-related activation-induced cytokine.

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