Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Apr 8;25(7):4120.
doi: 10.3390/ijms25074120.

The Golgi Apparatus: A Key Player in Innate Immunity

Ion Mărunţelu  1   2 , Alexandra-Elena Constantinescu  3   4 , Razvan-Adrian Covache-Busuioc  3 , Ileana Constantinescu  1   2   4   5
Affiliations
Review

The Golgi Apparatus: A Key Player in Innate Immunity

Ion Mărunţelu et al. Int J Mol Sci. .

Abstract

The Golgi apparatus, long recognized for its roles in protein processing and vesicular trafficking, has recently been identified as a crucial contributor to innate immune signaling pathways. This review discusses our expanding understanding of the Golgi apparatus's involvement in initiating and activating these pathways. It highlights the significance of membrane connections between the Golgi and other organelles, such as the endoplasmic reticulum, mitochondria, endosomes, and autophagosomes. These connections are vital for the efficient transmission of innate immune signals and the activation of effector responses. Furthermore, the article delves into the Golgi apparatus's roles in key immune pathways, including the inflammasome-mediated activation of caspase-1, the cGAS-STING pathway, and TLR/RLR signaling. Overall, this review aims to provide insights into the multifunctional nature of the Golgi apparatus and its impact on innate immunity.

Keywords: Golgi-apparatus; NLRP3-inflammasome; immunology; innate immunity; intracellular-signaling.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
The figure shows PLC releases Ca2+ from the ER through inositol-1, 4, 5-trisphosphate (InsP3) Receptor. Ca2+ accumulates in the mitochondria, which may lead to mitochondrial damage (1). Damaged mitochondria release calcium ions (Ca2+) that accumulate in the mitochondria-associated membranes (MAMs), contributing to their activation (1*). Damaged mitochondria release several factors that trigger the activation of the NLRP3 inflammasome (2). NLRP3 was shown to directly bind to mitochondria-associated ER membranes (MAMs) (black arrow). The other product of PLC activation, diacylglycerol (DAG), accumulates in the Golgi (3) and increases the activity of PKD (protein kinase D), which then phosphorylates NLRP3-Inflammasome and activates it (3*), releasing it from MAMs (4).
Figure 2
Figure 2
STING activates TBK1 at the Golgi. TBK1 phosphorylates interferon regulatory factor 3 (IRF3), leading to transcription of IFNb genes and stimulation of type I and III interferon genes as well as genes encoding proinflammatory cytokines and chemokines. STING is then degraded by the lysosomes through microautophagy.
See this image and copyright information in PMC

References

    1. Saceleanu V.M., Covache-Busuioc R.-A., Costin H.-P., Glavan L.-A., Ciurea A.V. An Important Step in Neuroscience: Camillo Golgi and His Discoveries. Cells. 2022;11:4112. doi: 10.3390/cells11244112. - DOI - PMC - PubMed
    1. Shorter J., Warren G. Golgi Architecture and Inheritance. Annu. Rev. Cell Dev. Biol. 2002;18:379–420. doi: 10.1146/annurev.cellbio.18.030602.133733. - DOI - PubMed
    1. Tang D., Wang Y. Cell Cycle Regulation of Golgi Membrane Dynamics. Trends Cell Biol. 2013;23:296–304. doi: 10.1016/j.tcb.2013.01.008. - DOI - PMC - PubMed
    1. Boncompain G., Weigel A.V. Transport and Sorting in the Golgi Complex: Multiple Mechanisms Sort Diverse Cargo. Curr. Opin. Cell Biol. 2018;50:94–101. doi: 10.1016/j.ceb.2018.03.002. - DOI - PubMed
    1. Sehgal P.B., Lee J.E. Protein Trafficking Dysfunctions: Role in the Pathogenesis of Pulmonary Arterial Hypertension. Pulm. Circ. 2011;1:17–32. doi: 10.4103/2045-8932.78097. - DOI - PMC - PubMed