Programmed Cell Death Pathways in the Pathogenesis of Systemic Lupus Erythematosus

Yang, Fengying; He, Yi; Zhai, Zeqing; Sun, Erwei

doi:10.1155/2019/3638562

Cited by 65 publications

(65 citation statements)

References 169 publications

(181 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Consequently, the ischemic injury directly induces program cell deaths of neutrophils, including NETosis, in several organs after renal injury (34). After the renal ischemia, cell apoptosis and NETosis might be exacerbated the lupus disease activity due to the lupus exacerbation from the program cell deaths (35). Because of the prominent responses against several stimulators of the Fcgr2b-/-mice (2,7,8), apoptosis and NETosis derived from renal I/R might be more profound than the responses in the normal mice.…”

Section: Introductionmentioning

confidence: 99%

Acute Kidney Injury Induced Lupus Exacerbation Through the Enhanced Neutrophil Extracellular Traps (and Apoptosis) in Fcgr2b Deficient Lupus Mice With Renal Ischemia Reperfusion Injury

et al. 2021

View full text Add to dashboard Cite

Renal ischemia is the most common cause of acute kidney injury (AKI) that might be exacerbate lupus activity through neutrophil extracellular traps (NETs) and apoptosis. Here, the renal ischemia reperfusion injury (I/R) was performed in Fc gamma receptor 2b deficient (Fcgr2b-/-) lupus mice and the in vitro experiments. At 24 h post-renal I/R injury, NETs in peripheral blood neutrophils and in kidneys were detected using myeloperoxidase (MPO), neutrophil elastase (NE) and citrullinated histone H3 (CitH3), as well as kidney apoptosis (activating caspase-3), which were prominent in Fcgr2b-/- mice more compared to wild-type (WT). After 120 h renal-I/R injury, renal NETs (using MPO and NE) were non-detectable, whereas glomerular immunoglobulin (Ig) deposition and serum anti-dsDNA were increased in Fcgr2b-/- mice. These results imply that renal NETs at 24 h post-renal I/R exacerbated the lupus nephritis at 120 h post-renal I/R injury in Fcgr2b-/- lupus mice. Furthermore, a Syk inhibitor attenuated NETs, that activated by phorbol myristate acetate (PMA; a NETs activator) or lipopolysaccharide (LPS; a potent inflammatory stimulator), more prominently in Fcgr2b-/- neutrophils than the WT cells as determined by dsDNA, PAD4 and MPO. In addition, the inhibitors against Syk and PAD4 attenuated lupus characteristics (serum creatinine, proteinuria, and anti-dsDNA) in Fcgr2b-/- mice at 120 h post-renal I/R injury. In conclusion, renal I/R in Fcgr2b-/- mice induced lupus exacerbation at 120 h post-I/R injury partly because Syk-enhanced renal NETs led to apoptosis-induced anti-dsDNA, which was attenuated by a Syk inhibitor.

show abstract

Section: Introductionmentioning

confidence: 99%

Acute Kidney Injury Induced Lupus Exacerbation Through the Enhanced Neutrophil Extracellular Traps (and Apoptosis) in Fcgr2b Deficient Lupus Mice With Renal Ischemia Reperfusion Injury

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Necroptosis is a programmed form of necrosis, or inflammatory cell death, so it possesses the characteristics of both apoptotic and necrotic cell death. In particular, the nuclear material released during the process of necroptosis seems to be more immunogenic than the apoptotic material [ 24 ]. This explains our experimental results well, so we cannot rule out the fact that CM-EE induces necroptosis.…”

Section: Discussionmentioning

confidence: 99%

Cordyceps militaris Induces Immunogenic Cell Death and Enhances Antitumor Immunogenic Response in Breast Cancer

Quan

Kwak

Lee

et al. 2020

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Cordyceps militaris has been widely used as a traditional medicine in East Asia. Its effects against breast cancer have been reported previously. However, whether C. militaris-induced breast cancer cell death is immunogenic remains unelucidated. This study aimed to determine whether ethanolic extracts of C. militaris (CM-EE) could induce immunogenic cell death (ICD) in breast cancer immunotherapy to improve the efficacy of immune checkpoint inhibitors. Human and mouse breast cancer cells were treated with various concentrations of CM-EE for 72 h, and cytotoxicity was measured using the sulforhodamine B assay. Flow cytometry was used to assess cell death with annexin V/7-AAD staining and measure the surface exposure of damage-associated molecular pattern (DAMP) molecules including calreticulin, HSP70, and HSP90. Western blot for cleaved poly (ADP-ribose) polymerase (PARP) was used to confirm apoptotic cell death. The immunogenicity of CM-EE-induced dead cells was evaluated using the CFSE dilution assay. CM-EE reduced the viability of human (MCF7, MDA-MB-231, HS578T, and SKBR3) and mouse (4T1-neu-HA, TUBO-HA, and TUBO-P2J-HA) breast cancer cells. The IC50 was 25–50 µg/ml in human breast cancer cells and 10–50 µg/ml in mouse breast cancer cells at 72 h. CM-EE-treated breast cancer cells were positively stained by annexin V, cleaved PARP, and cleaved caspase 3/7 which were increased upon CM-EE treatment. Surface exposure of DAMP molecules was increased in dose- and time-dependent manners. The CFSE dilution assay revealed that dendritic cells fed with CM-EE-treated breast cancer cells successfully stimulated tumor-specific T cell proliferation without inhibiting DC function and T cell proliferation. The expression of PD-L1 mRNA and protein level was increased in dose-dependent manners. In addition, CM-EE also potentiated the cytotoxic activity of tumor-specific T cells. CM-EE can induce immunogenic and apoptotic cell death in breast cancer cells, and it is a good candidate for cancer immunotherapy and may improve the efficacy of immune checkpoint inhibitors.

show abstract

“…Although the focus was on the effects of pathogens in inducing pyroptosis, noninfectious disorders such as systemic lupus erythematosus (SLE) where anti‐dsDNA activates NLRP3 inflammasomes and in turn mediates pyroptosis that plays an important role in the pathogenesis and progression of SLE 80 . Another example of DAMPs activating pyroptosis is in trauma, which is leading cause of death worldwide.…”

Section: Major Players Of the Pyroptosis Processmentioning

confidence: 99%

Pyroptosis: The missing puzzle among innate and adaptive immunity crosstalk

Hachim

Khalil

Elemam

et al. 2020

Journal of Leukocyte Biology

View full text Add to dashboard Cite

Pyroptosis is a newly discovered programmed cell death with inflammasome formation. Pattern recognition receptors that identify repetitive motifs of prospective pathogens such as LPS of gram‐negative bacteria are crucial to pyroptosis. Upon stimulation by pathogen‐associated molecular patterns or damage‐associated molecular patterns, proinflammatory cytokines, mainly IL‐1 family members IL‐1β and IL‐18, are released through pyroptosis specific pore‐forming protein, gasdermin D. Even though IL‐1 family members are mainly involved in innate immunity, they can be factors in adaptive immunity. Given the importance of IL‐1 family members in health and diseases, deciphering the role of pyroptosis in the regulation of innate and adaptive immunity is of great importance, especially with the recent progress in identifying the exact mechanism of such a pathway. In this review, we will focus on how the innate inflammatory mediators can regulate the adaptive immune system and vice versa via pyroptosis.

show abstract

Programmed Cell Death Pathways in the Pathogenesis of Systemic Lupus Erythematosus

Cited by 65 publications

References 169 publications

Acute Kidney Injury Induced Lupus Exacerbation Through the Enhanced Neutrophil Extracellular Traps (and Apoptosis) in Fcgr2b Deficient Lupus Mice With Renal Ischemia Reperfusion Injury

Acute Kidney Injury Induced Lupus Exacerbation Through the Enhanced Neutrophil Extracellular Traps (and Apoptosis) in Fcgr2b Deficient Lupus Mice With Renal Ischemia Reperfusion Injury

Cordyceps militaris Induces Immunogenic Cell Death and Enhances Antitumor Immunogenic Response in Breast Cancer

Pyroptosis: The missing puzzle among innate and adaptive immunity crosstalk

Contact Info

Product

Resources

About