APRIL polymorphism and systemic lupus erythematosus (SLE) susceptibility

Lee, Young Ho; Ota, Fumie; Kim-Howard, Xana; Kaufman, Kenneth M.; Nath, Swapan K.

doi:10.1093/rheumatology/kem093

Cited by 25 publications

(13 citation statements)

References 13 publications

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“…Polymorphisms in the APRIL and BAFF genes TNFSF13 and TNFSF13B have been shown to be associated with the autoimmune phenotype of SLE in humans (42)(43)(44). Although monocytes carrying the 871T polymorphism in the promoter region of TNFSF13B expressed significantly higher levels of BAFF, no significant association with susceptibility to SLE was observed.…”

Section: Discussionmentioning

confidence: 99%

Systemic activation of the immune system induces aberrant BAFF and APRIL expression in B cells in patients with systemic lupus erythematosus

Chu¹,

Enghard²,

Schürer³

et al. 2009

Arthritis & Rheumatism

105

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Section: Discussionmentioning

confidence: 99%

Systemic activation of the immune system induces aberrant BAFF and APRIL expression in B cells in patients with systemic lupus erythematosus

Chu¹,

Enghard²,

Schürer³

et al. 2009

Arthritis & Rheumatism

105

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“…Interestingly, polymorphisms of the BAFF gene promoter region have been detected with a high frequency in patients with SLE and idiopathic thrombocytopenic purpura [47,48]. APRIL serum levels have also been found to be increased in autoimmune diseases and some polymorphisms associated with SLE [49][50][51][52].…”

Section: B Cell Activator Factor and A Proliferation-inducing Ligand mentioning

confidence: 99%

B cell activator factor and a proliferation-inducing ligand at the cross-road of chronic lymphocytic leukemia and autoimmunity

Ferrer

Hodgson

Montserrat

et al. 2009

Leukemia & Lymphoma

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The combination of the neoplastic accumulation of mature B lymphocytes with the presence of autoimmune phenomena is a characteristic finding in chronic B cell lymphoproliferative disorders, particularly chronic lymphocytic leukemia. Identification of mechanisms linking neoplasia to the autoimmune defects is important for a better understanding and improving the treatment of these conditions. Among such mechanisms, the B cell activator factor (BAFF) and a proliferation-inducing ligand (APRIL), two members of the tumor necrosis factor family, play an important role. BAFF and APRIL have both been associated with autoimmunity, with their underlying mechanism of action most likely being related to the rescue of autoreactive B cells. In addition, BAFF and APRIL are crucial in B cell development and homeostasis particularly via the activation of NF-kappaB pathway-mediated survival signals. These two proteins, therefore, constitute a paradigm of pathophysiological defects linking neoplasia and autoimmunity, thereby providing a better understanding of chronic B cell lymphoproliferative disorders.

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“…This association was also replicated in a study on mixed European-American, African-American and Hispanic populations. 29 Thus, TNFSF13 is also an established susceptibility gene to SLE.…”

Section: Introductionmentioning

confidence: 99%

Cumulative association of eight susceptibility genes with systemic lupus erythematosus in a Japanese female population

et al. 2011

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Although large-scale studies established many susceptibility genes to systemic lupus erythematosus (SLE), effect of each gene is not sufficiently large to be used alone to identify individuals with strong genetic predisposition. In this study, we analyzed the cumulative number of risk alleles at eight established susceptibility loci, HLA-DRB1, IRF5, STAT4, BLK, TNFAIP3, TNIP1, FCGR2B and TNFSF13, in 282 Japanese female SLE and 222 healthy female controls. The average number of risk alleles was significantly increased in SLE (8.07 ± 1.60) than healthy controls (7.02 ± 1.64) (P¼1.63Â10 À12 ). Significant gene-gene interaction was not detected. When the subjects carrying seven risk alleles were used as a reference, the odds ratio (OR) for individuals carrying 10 and 11-13 risk alleles were 4.17 (95% confidence interval (CI) 1.89-9.19, P¼0.0002) and 8.77 (95% CI 1.92-40.0, P¼0.0016), respectively. In contrast, subjects with p4 risk alleles were significantly decreased in SLE (OR 0.15, CI 0.03-0.67, P¼0.007). The proportion of the patients with neurologic disorder was significantly increased in those carrying X10 risk alleles than those with o10 (OR 2.30, CI 1.09-4.83, P¼0.025). This study suggested that the cumulative number of risk alleles may efficiently distinguish groups with high and low genetic predisposition to SLE and its severe manifestation.

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APRIL polymorphism and systemic lupus erythematosus (SLE) susceptibility

Cited by 25 publications

References 13 publications

Systemic activation of the immune system induces aberrant BAFF and APRIL expression in B cells in patients with systemic lupus erythematosus

Systemic activation of the immune system induces aberrant BAFF and APRIL expression in B cells in patients with systemic lupus erythematosus

B cell activator factor and a proliferation-inducing ligand at the cross-road of chronic lymphocytic leukemia and autoimmunity

Cumulative association of eight susceptibility genes with systemic lupus erythematosus in a Japanese female population

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