2019
DOI: 10.2174/1871523018666181128161828
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Systemic Lupus Erythematosus: Symptoms and Signs at Initial Presentations

Abstract: Background: Systemic Lupus Erythematosus (SLE) is an autoimmune multisystem inflammatory condition that causes microvascular inflammation with the production of various auto-antibodies that play a major role in its pathogenesis. SLE can affect both sexes, all ages, and all ethnic groups with widespread geographical and socioeconomic backgrounds. Asia encompasses people of many sociocultural backgrounds with diverse ethnic. Objective: Due to a lack of national epidemiological research, the incidence and preva… Show more

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Cited by 21 publications
(20 citation statements)
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“…: mitochondrial hyperpolarization and the death of T cells [17][18][19]; activation of Rho-associated protein kinase (ROCK) which further mediates the binding of IL17 transcription enhancer interferon regulatory factor 4 (IRF4) [20]; dephosphorylation of cAMP-responsive element-binding protein 1 (CREB), resulting in suppression of IL2 transcription (mediated by downregulation of expression of MAPK-mitogen-activated protein kinase and DNMT1-DNA methyl transferase 1) [21]. Further upregulation of IL17 and downregulation of IL2 production is mediated by calcium/calmodulin-dependent protein kinase IV (CaMKIV), which in turn increases the binding of cAMP response element modulator (CREMα) [12][13][14][15][16][17][18]. Certain co-stimulatory signaling molecules such as ICOS (Inducible T cell co-stimulator), PI3K (phosphoinositide 3-kinase) and mTOR (mechanistic target of Rapamycin) also aid in similar interleukin regulation [12].…”
Section: Introductionmentioning
confidence: 99%
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“…: mitochondrial hyperpolarization and the death of T cells [17][18][19]; activation of Rho-associated protein kinase (ROCK) which further mediates the binding of IL17 transcription enhancer interferon regulatory factor 4 (IRF4) [20]; dephosphorylation of cAMP-responsive element-binding protein 1 (CREB), resulting in suppression of IL2 transcription (mediated by downregulation of expression of MAPK-mitogen-activated protein kinase and DNMT1-DNA methyl transferase 1) [21]. Further upregulation of IL17 and downregulation of IL2 production is mediated by calcium/calmodulin-dependent protein kinase IV (CaMKIV), which in turn increases the binding of cAMP response element modulator (CREMα) [12][13][14][15][16][17][18]. Certain co-stimulatory signaling molecules such as ICOS (Inducible T cell co-stimulator), PI3K (phosphoinositide 3-kinase) and mTOR (mechanistic target of Rapamycin) also aid in similar interleukin regulation [12].…”
Section: Introductionmentioning
confidence: 99%
“…Autoantibodies against the nuclear body, ribonucleoproteins and DNA are formed in SLE. Moreover, the immunological and hematopoietic cells of the body are also attacked by autoantibodies, thereby causing severe damage to the blood cells as reflected by hemolytic anemia, leukopenia and thrombocytopenia [17]. Further secondary manifestations are also observed wherein the vital organs such as the liver, heart, lungs and kidneys undergo acute failure, thereby increasing morbidity and mortality ( Figure 2).…”
Section: Introductionmentioning
confidence: 99%
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“…The systematic lupus erythematosus (SLE) is a multisystem autoimmune disease with diverse clinical presentations. 1 The pathogenesis of SLE is complex and undefined, with evidence of the interaction of several genetic and environmental causes. 2 MicroRNAs (miRNAs) are short, evolutionary conserved, single-stranded noncoding RNAs with approximately 22 nucleotides in length derived from large primary transcript encoded by their host genes.…”
Section: Introductionmentioning
confidence: 99%
“…The systematic lupus erythematosus (SLE) is a multisystem autoimmune disease with diverse clinical presentations 1 . The pathogenesis of SLE is complex and undefined, with evidence of the interaction of several genetic and environmental causes 2 …”
Section: Introductionmentioning
confidence: 99%