scholarly journals Meta-analysis of programmed cell death 1 polymorphisms with systemic lupus erythematosus risk

Oncotarget ◽  
2017 ◽  
Vol 8 (22) ◽  
pp. 36885-36897 ◽  
Author(s):  
Jie Gao ◽  
Nan Gai ◽  
Li Wang ◽  
Kang Liu ◽  
Xing-Han Liu ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Lupus Erythematosus ◽  
Meta Analysis ◽  
Systemic Lupus ◽  
Programmed Cell Death 1

Programmed cell death 1 gene polymorphism as a possible risk for systemic lupus erythematosus in Egyptian females

Lupus ◽  
2019 ◽  
Vol 28 (12) ◽  
pp. 1427-1434
Author(s):  
S M Abo El-khair ◽  
W Sameer ◽  
N Awadallah ◽  
D Shaalan
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Lupus Erythematosus ◽  
Nucleotide Polymorphisms ◽  
Systemic Lupus ◽  
Retrospective Case ◽  
Allelic Discrimination ◽  
Female Population ◽  
Programmed Cell Death 1

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with a suggested genetic basis. The newly identified human programmed cell death 1 gene could be associated with SLE susceptibility. We aimed to investigate the association between programmed cell death 1 polymorphism (PD1.3G/A (rs11568821) and PD1.5C/T (rs2227981)) with the risk of SLE in the Egyptian female population. This retrospective case–control study included 150 Egyptian females; 70 patients diagnosed to have SLE and 80 age-matched healthy controls. The two single nucleotide polymorphisms of the pdcd1 gene were genotyped by allelic discrimination through TaqMan real-time polymerase chain reaction. The PD1.3GG genotype and G allele as well as the PD1.5CC genotype were significantly more frequent in SLE patients (67.1%; p = 0.023, 82.1%; p = 0.0021, 62.9%; p = 0.0287 respectively). The GC haplotype was the most common haplotype among SLE patients (70.77%) with a reported significant linkage disequilibrium between the two studied polymorphisms ( p = 0.0041). Although most of the studies showed significant association of SLE with the minor alleles, we reported a significant association between the dominant genotypes (PD1.3GG and PD1.5CC) as well as the major G allele with the risk of SLE among Egyptian females.

Effects of the programmed cell death 1 (PDCD1) polymorphisms in susceptibility to systemic lupus erythematosus

2019 ◽  
Vol 47 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Farshid Fathi ◽  
Erfan Sadeghi ◽  
Noushin Lotfi ◽  
Hossein Hafezi ◽  
Meysam Ahmadi ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Programmed Cell Death 1

Serum levels of soluble programmed cell death protein 1 and soluble programmed cell death protein ligand 2 are increased in systemic lupus erythematosus and associated with the disease activity

Lupus ◽  
2020 ◽  
Vol 29 (7) ◽  
pp. 686-696
Author(s):  
Shinya Hirahara ◽  
Yasuhiro Katsumata ◽  
Hidenaga Kawasumi ◽  
Yashushi Kawaguchi ◽  
Masayoshi Harigai
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Disease Activity ◽  
Lupus Erythematosus ◽  
Serum Levels ◽  
Healthy Controls ◽  
Systemic Lupus ◽  
Dsdna Antibodies ◽  
Cell Death Protein

Objective Programmed cell death protein 1 (PD-1) pathway plays important roles in systemic lupus erythematosus (SLE). We aimed to elucidate the association of serum soluble PD-1 (sPD-1) and related molecules with SLE and to explore their usefulness as biomarkers. Methods We retrospectively measured the serum levels of sPD-1, soluble PD-ligand 1 (sPD-L1), soluble PD-ligand 2 (sPD-L2) and interleukin (IL)-21 by ELISA in SLE patients, systemic sclerosis patients and healthy controls. Repeat sera samples were also obtained post treatment. Results The serum levels of sPD-1 and sPD-L2 in SLE patients with high disease activity were significantly higher than those in SLE patients with low disease activity, systemic sclerosis patients and healthy controls ( n = 58, 15, 20 and 21, respectively; p < 0.001). However, the serum levels of sPD-L1 and IL-21 were not elevated in SLE patients. The serum levels of sPD-1 and sPD-L2 were higher among active SLE patients who tested positive for anti-dsDNA antibodies than in those who tested negative ( p = 0.002 and <0.001, respectively). There were moderate correlations between the serum levels of sPD-1 and sPD-L2 and the SLE Disease Activity Index 2000 scores, the titres of anti-dsDNA antibodies and the serum levels of complements. Furthermore, the serum levels of sPD-1 and sPD-L2 decreased significantly in accordance with disease amelioration following treatment ( p < 0.001). Conclusion The present study demonstrated the association of serum sPD-1 and sPD-L2 with SLE and suggests their usefulness as disease activity biomarkers for SLE.

scholarly journals Programmed Cell Death Pathways in the Pathogenesis of Systemic Lupus Erythematosus

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Fangyuan Yang ◽  
Yi He ◽  
Zeqing Zhai ◽  
Erwei Sun
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Responses ◽  
Lupus Erythematosus ◽  
Tissue Damage ◽  
Systemic Lupus ◽  
Secondary Necrosis ◽  
Cell Death Pathways

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease characterized by excessive inflammatory and immune responses and tissue damage. Increasing evidence has demonstrated the important role of programmed cell death in SLE pathogenesis. When apoptosis encounters with defective clearance, accumulated apoptotic cells lead to secondary necrosis. Different forms of lytic cell death, including secondary necrosis after apoptosis, NETosis, necroptosis, and pyroptosis, contribute to the release of damage-associated molecular patterns (DAMPs) and autoantigens, resulting in triggering immunity and tissue damage in SLE. However, the role of autophagy in SLE pathogenesis is in dispute. This review briefly discusses different forms of programmed cell death pathways and lay particular emphasis on inflammatory cell death pathways such as NETosis, pyroptosis, and necroptosis and their roles in the inflammatory and immune responses in SLE.

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