| name | description | evidence |
|---|---|---|
| Discoid Lupus Erythematosus | Primarily affects the skin. | TRUNCATED |
| Neonatal Lupus | Affects infants, caused by transplacental transfer of maternal autoantibodies. | TRUNCATED |
| Drug-Induced Lupus | Caused by certain medications and usually reversible. | TRUNCATED |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:27709413 | PARTIAL | Here, we review what is known on the altered metabolic patterns of CD4(+) T cells, B cells, and myeloid cells in lupus patients and lupus-prone mice and how they contribute to lupus pathogenesis. | The reference discusses the altered metabolic patterns of B cells, CD4(+) T cells, and myeloid cells (which include macrophages) and their contribution to lupus, which indirectly supports the involvement of these cell types in lupus mechanisms, but it does not specifically address immune complex formation directly. |
| PMID:29925508 | PARTIAL | TLR4(+)CXCR4(+) plasma cells drive nephritis development in systemic lupus erythematosus. | This reference demonstrates the role of specific plasma cells in the development of lupus nephritis, implying their role in immune complex-related pathology, but does not detail the direct involvement of B cells or macrophages in immune complex formation. |
| PMID:34402453 | PARTIAL | B-lymphocytes are crucial in the pathogenesis of systemic lupus erythematosus (SLE), including autoantibody production, antigen presentation, co-stimulation, and cytokine secretion. | The reference highlights the crucial role of B cells in the pathogenesis of SLE through mechanisms such as autoantibody production, which is critical for immune complex formation. However, it does not explicitly discuss the role of plasma cells or macrophages in the context given. |
| PMID:22999705 | PARTIAL | C1q opsonized apoptotic cells also exert an immunosuppressive effect through cytokine regulation and the stimulation of additional opsonins by macrophages. | This suggests that macrophages have a role in immune complex-mediated processes through cytokine regulation and opsonin stimulation, contributing to the immune system’s activity in lupus but does not detail the involvement of B cells or plasma cells in immune complex formation. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:16572034 | PARTIAL | Systemic lupus erythematosus is an autoimmune disease that causes inflammation in the tissues of the brain, endothelial cells, gastrointestinal/genitourinary (GI/GU), joints, kidneys, muscles, and skin. Lupus comprises a range of multisystem disorders involving the deposition of aberrant immune complexes into tissues. | The literature confirms the deposition of immune complexes in kidneys, joints, and skin, but does not mention the heart and lung specifically in this context. |
| PMID:33841392 | PARTIAL | Systemic lupus erythematosus (SLE) is a complex chronic autoimmune disease characterized by tissue damage and widespread inflammation in response to environmental challenges. Deposition of immune complexes in kidneys glomeruli are associated with lupus nephritis, determining SLE diagnosis. | The literature supports the deposition of immune complexes in kidney glomeruli but does not cover skeletal joints, skin, heart, or lung in this context. |
| PMID:30009962 | SUPPORT | LN is characterized by glomerular kidney injury, essentially due to deposition of immune complexes involving autoantibodies against cellular components and circulating proteins. | This confirms immune complex deposition in kidneys. |
| PMID:2860699 | SUPPORT | Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis. | This confirms immune complex deposition in the heart. |
| PMID:28900675 | WRONG_STATEMENT | Recent studies demonstrated an increased incidence of osteoporosis and peripheral and vertebral fractures in patients with systemic lupus erythematosus (SLE). | This reference does not mention the deposition of immune complexes in skeletal joints. |
| PMID:158982 | SUPPORT | Abundant evidence currently exists to suggest that immune complexes play an important role in inflammatory diseases of the lung. ... systemic lupus erythematosus have been shown to be associated with the presence of immune complexes both in lung and in the serum. | This confirms immune complex deposition in the lung. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:22192660 | SUPPORT | Systemic lupus erythematosus is a prototypic autoimmune disease characterized by autoantibody production and immune complex formation/deposition in target organs such as the kidney. Resultant local inflammation then leads to organ damage. | The article describes inflammation and immune complex deposition as mechanisms leading to tissue damage in SLE. |
| PMID:36555640 | SUPPORT | The clinical heterogeneity of the disease is accompanied by complex disturbances affecting the immune system with inflammation and tissue damage due to loss of tolerance to nuclear antigens and the deposition of immune complexes in tissues. | The literature explains that inflammation and tissue damage are core mechanisms in the pathology of SLE due to immune system disturbances. |
| PMID:28623084 | SUPPORT | Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting multiple organs. A complex interaction of genetics, environment, and hormones leads to immune dysregulation and breakdown of tolerance to self-antigens, resulting in autoantibody production, inflammation, and destruction of end-organs. | This article outlines inflammation as part of the immune dysregulation in SLE, leading to tissue damage in multiple organs. |
| PMID:33841392 | SUPPORT | Systemic lupus erythematosus (SLE) is a complex chronic autoimmune disease characterized by tissue damage and widespread inflammation in response to environmental challenges. | The study identifies widespread inflammation and tissue damage as defining characteristics of SLE. |
| PMID:37712757 | SUPPORT | In the current review, we focus on the commonly affected organs (skin, kidney, and nervous system) in SLE to summarize the emerging biomarkers that show promise in disease diagnosis, monitoring and treatment response assessment. | The review supports that inflammation and tissue damage are significant mechanisms in SLE affecting organs such as the skin, kidneys, and nervous system. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:16572034 | SUPPORT | Systemic lupus erythematosus is an autoimmune disease that causes inflammation in the tissues... | The abstract confirms that inflammation is a key aspect of systemic lupus erythematosus pathogenesis. |
| PMID:26330673 | SUPPORT | Systemic lupus erythematosus, the prototype systemic autoimmune disease, is characterized by extensive self-reactivity, inflammation, and organ system damage. | The abstract clearly mentions inflammation as a characteristic feature of SLE. |
| PMID:32237942 | SUPPORT | Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that is potentially life-threatening and can affect any organ. | The literature describes SLE as a chronic autoimmune disease affecting various organs, implying sustained inflammation over time. |
| PMID:24992143 | SUPPORT | Recent evidence suggests that the inflammasome machinery is dysregulated in SLE, plays an important role in promotion of organ damage, and may mediate cross-talk between environmental triggers and the development of lupus. | The abstract discusses the role of inflammasome and inflammation in organ damage associated with SLE, supporting the chronic inflammation mechanism. |
| PMID:36555640 | SUPPORT | The clinical heterogeneity of the disease is accompanied by complex disturbances affecting the immune system with inflammation and tissue damage due to loss of tolerance to nuclear antigens and the deposition of immune complexes in tissues. | The literature describes inflammation and tissue damage due to immune complexes, which supports chronic inflammation as a mechanism of SLE. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:26951252 | SUPPORT | These include exposure to UV light, infections, certain hormones, and drugs which may activate the innate and adaptive immune system, resulting in inflammation, cytotoxic effects, and clinical symptoms. | This reference mentions the potential triggers for lupus flares, which include UV light (sunlight) and infections. |
| PMID:26494589 | SUPPORT | Some triggers for these exacerbations have been identified, including infections, vaccines, pregnancy, environmental factors such as weather, stress and drugs. | This reference specifically states that stress and infections can trigger lupus flares. |
| PMID:22385883 | SUPPORT | Exposure to sunlight is one of the environmental factors involved in the pathogenesis of systemic lupus erythematosus. | This reference confirms that sunlight exposure can trigger lupus flares. |
| PMID:30488801 | SUPPORT | The cutaneous manifestations that were present included malar rash 37.69%, photosensitivity 35.10%, discoid lupus 17.63%, and hair loss 39.29%. | This reference discusses photosensitivity (sunlight) as a significant factor, aligning with the statement's mention of sunlight as a trigger. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:23846232 | PARTIAL | The most common clinical manifestations were malar rash (61.3%)... | The literature supports that malar rash is a common manifestation of systemic lupus erythematosus (SLE), but it does not specifically categorize it under 'Cutaneous'. |
| PMID:16966017 | PARTIAL | There are 3 forms of cutaneous lupus: chronic cutaneous (discoid) lupus, subacute cutaneous lupus, and acute cutaneous lupus. | This reference discusses cutaneous forms of lupus but does not specifically mention malar rash as one of these types. |
| PMID:17711886 | PARTIAL | The common symptoms of SLE in children and adolescents include... rash... | This reference indicates that rash, which can include malar rash, is common in SLE, but it does not specifically categorize malar rash as 'Cutaneous'. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:15379880 | SUPPORT | Photosensitivity is one the most common manifestations of lupus erythematosus. | The literature directly mentions that photosensitivity is a common manifestation in lupus erythematosus, supporting the statement that it is a frequent phenotype. |
| PMID:30858846 | NO_EVIDENCE | No relevant information regarding photosensitivity in systemic lupus erythematosus was found in the provided summary. | None |
| PMID:31909888 | PARTIAL | Fatigue, widespread pain, sleep dysfunction, and mood disorders are common symptoms in SLE. | While this reference mentions common symptoms of SLE, it does not specifically address photosensitivity. |
| PMID:30988213 | PARTIAL | The cutaneous manifestations of lupus erythematosus (LE) include LE-specific and LE-nonspecific skin lesions. | The reference discusses cutaneous manifestations of LE but does not specifically highlight photosensitivity. |
| PMID:31575058 | PARTIAL | The development of SLE is attributed to the breach of immunological tolerance and the interaction between SLE-susceptibility genes and various environmental factors. | While the reference discusses factors contributing to the development of SLE, it does not explicitly address photosensitivity. |
| PMID:23846232 | PARTIAL | The most common clinical manifestations were malar rash (61.3%), arthritis (52.3%), haematological disease (51.6%), oral ulcers (51%) and renal disease (40.6%). | Photosensitivity is not specifically mentioned among the most common clinical manifestations in this study. |
| PMID:29087262 | SUPPORT | Analysis revealed that photosensitivity, nephritis and thrombocytopenia were negatively associated with familial SLE. | This reference suggests that photosensitivity is common in non-familial SLE, indirectly supporting the statement regarding its frequency. |
| PMID:37236713 | NO_EVIDENCE | No specific mention of photosensitivity in the provided summary. | None |
| PMID:34160552 | NO_EVIDENCE | No specific mention of photosensitivity in the provided summary. | None |
| PMID:8398608 | NO_EVIDENCE | No specific mention of photosensitivity in the provided summary. | None |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:19591780 | SUPPORT | Arthritis in systemic lupus erythematosus (SLE) is one of the most common disease manifestations. Nearly all joints can be affected by SLE, but hand and knee involvement are the most typical. | This reference explicitly states that arthritis is one of the most common disease manifestations in patients with SLE. |
| PMID:27742023 | SUPPORT | The precise nature of the disorder can be obscure and different disorders can present with similar symptoms, such as joint pain. | The statement mentions joint pain, which is associated with arthritis and suggests that musculoskeletal symptoms are common in SLE. |
| PMID:19013374 | SUPPORT | Systemic lupus erythematosus is an autoimmune and inflammatory disease characterized by a variety of symptoms, including arthropathy. The clinical presentation of joint involvement varies, ranging from arthralgia without erosions or deformity to an erosive arthropathy and severe functional disability. | This reference elaborates on the different forms of joint involvement in SLE, including arthropathy, which reinforces the statement that arthritis is a common musculoskeletal phenotype in SLE. |
| PMID:32956154 | SUPPORT | Polyautoimmunity was recorded in 15 patients with RA (13.8%), 43 with SLE (41%), and 2 controls (2.2%). ... In SLE, joint damage (OR, 2.282; p = 0.038) and anti-RNP antibodies (OR, 5.095; p = 0.028) were risk factors for polyautoimmunity... | This reference indicates a significant association between SLE and joint damage, further supporting the statement. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:36251502 | SUPPORT | Among 365 patients with SLE, 36% had LN. | The study indicates that a significant portion of patients with Systemic Lupus Erythematosus (SLE) exhibit kidney involvement in the form of lupus nephritis (LN). |
| PMID:330103 | SUPPORT | The pathologic abnormalities present in patients with SLE have been classified as follows: minimal lupus nephritis, mild (focal) proliferative lupus nephritis, severe (diffuse) proliferative lupus nephritis, and membranous lupus nephritis. | The classification of pathologic abnormalities in SLE patients includes various forms of lupus nephritis, which confirms kidney involvement. |
| PMID:30454753 | SUPPORT | Patients with early onset SLE tend to have a greater genetic component to their disease cause, more multisystemic involvement, and a more severe disease course, which includes greater risks for developing nephritis and end-stage kidney disease. | This study highlights that childhood-onset SLE has a high risk of developing nephritis, underlining kidney involvement as a significant phenotype. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:34459313 | PARTIAL | Introduction: Systemic lupus erythematosus (SLE) may present with features of several systems, including hematological manifestations. Concomitant renal involvement and low C3 levels were significantly more frequent in patients with hematological involvement. | This study suggests that hematological involvement and kidney involvement can be concomitant in SLE patients, but they are not categorized together as a single phenotype of SLE. |
| PMID:32725543 | NO_EVIDENCE | Kidney involvement occurs in over 50% of children and treatment decisions are guided by the histological classification. | The study discusses kidney involvement in pediatric SLE but does not categorize it as "Hematologic phenotype". |
| PMID:22312827 | NO_EVIDENCE | Systemic lupus erythematosus (SLE) is a chronic syndrome with unknown etiology and polymorphic clinical picture... Severe SLE involves glomerulonephritis, complications in the central nervous system, cardiac and pulmonary complications and major changes in the blood. | The literature describes both hematologic changes and kidney involvement separately but does not categorically combine them into a single phenotype. |
| PMID:14717922 | NO_EVIDENCE | The currently used classification reflects our understanding of the pathogenesis of the various forms of lupus nephritis... The diagnosis should also include entries for any concomitant vascular or tubulointerstitial lesions. | This paper details the classification of lupus nephritis but does not mention it as a hematologic phenotype. |
| PMID:36251502 | NO_EVIDENCE | CONCLUSION: This study aids in the recognition of the demographic, clinical, laboratory features, and the histological patterns of LN patients in Saudi Arabia, that probably has a role in the development and disease progression. | This study focuses on the prevalence and patterns of lupus nephritis but does not treat it as a hematologic phenotype. |
| name | presence | evidence | specificity | frequency | notes |
|---|---|---|---|---|---|
| Anti-Nuclear Antibodies (ANA) | Positive | TRUNCATED | High | 98% | None |
| Anti-dsDNA Antibodies | Positive | TRUNCATED | High | None | None |
| Anti-Smith Antibodies | Positive | TRUNCATED | High | None | None |
| Anti-Histone Antibodies | Positive | TRUNCATED | None | None | Common in drug-induced lupus. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:37801591 | SUPPORT | HLA-DR2 was significantly more frequently found in SLE patients than in controls (odds ratio [OR] = 2.05, 95% CI, 1.44-2.92, p < 0.001)... HLA-DR2 patients had an earlier onset of disease as well as a higher prevalence of oral ulcer, avascular necrosis of bone, and renal involvement (lupus nephritis). | The study indicates that HLA-DR2 is associated with an increased susceptibility to SLE in the Taiwanese population. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:25546242 | SUPPORT | HLA-DR3 , DR9, DR15 were potent risk factors for SLE (1.88 [1.58, 2.23], P < 0.001; 1.24 [1.07, 1.45], P < 0.05; 1.25 [1.10, 1.43], P < 0.001, respectively). | The study provides evidence that HLA-DR3 is a potent risk factor for systemic lupus erythematosus (SLE), supporting the statement. |
| PMID:17910142 | PARTIAL | A positive HLA-DR3 anti-Ro/La antibody association was found in the patients with SLE (9/21, 43% vs 5/55, 9%; odds ratio (OR) = 7.5; CP = 0.01). | The study finds a significant association between HLA-DR3 and the presence of anti-Ro/La antibodies in SLE patients, though it does not establish that HLA-DR3 alone is a genetic risk factor for SLE. |
| PMID:6103441 | NO_EVIDENCE | It was also noted that the distribution of DR antigens in the hydralazine-SLE patients was significantly different from that in the group with idiopathic SLE. | This study highlights differences in HLA-DR distribution between drug-induced SLE and idiopathic SLE, but it does not specifically address the genetic contribution of HLA-DR3 to idiopathic SLE. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:31232672 | SUPPORT | We found that the PTPN22 polymorphisms rs1310182 A allele (p = 0.01, OR = 1.92 95% CI = 1.16-3.18), and rs1310182 AA genotype with (p < 0.001) and rs12760457 TT (p = 0.046) were associated with PSLE. | The study indicates that certain polymorphisms in the PTPN22 gene are associated with pediatric systemic lupus erythematosus (PSLE), supporting the genetic association between PTPN22 and SLE. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:23912645 | SUPPORT | Our results showed a significant association between rs7574865 T allele (odds ratio (OR) = 1.50, 95 % CI = 1.18-1.92, P = 0.002) and susceptibility to SLE. | The study found a significant association between the STAT4 gene (specifically rs7574865) and susceptibility to SLE. |
| PMID:31082500 | SUPPORT | Analysis of existing transcriptomes and GWAS data identified eight up-regulated candidate genes with more than four relationships among the different pathways associated with SNPs to pinpoint the relevant loci linked to SLE... STAT4... | This study identified STAT4 as one of the candidate genes associated with SLE through transcriptomic data analysis and pathway analysis of GWAS data. |
| PMID:34525002 | SUPPORT | The main objective of this study was to evaluate an association between HLA, STAT4, IRF5, and BLK polymorphisms and the presence of JA in Brazilian individuals with SLE. METHODS: Patients were selected from a cohort of individuals with SLE followed at 2 rheumatology reference centers in Salvador, Bahia, Brazil. | The study aimed to evaluate the association between STAT4 polymorphisms and the presence of Jaccoud Arthropathy in individuals with SLE, implying an association between STAT4 and SLE. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:20962850 | SUPPORT | Our results replicate previously reported associations to alleles of interferon regulatory factor 5 (IRF5)... This study confirms the existence of multiple genetic risk factors for SLE... | The study clearly identifies IRF5 as one of the genetic risk factors associated with SLE. |
| PMID:26233721 | SUPPORT | This meta-analysis demonstrated the IRF5 rs2070197 polymorphism conferred susceptibility to SLE in all subjects... The IRF5 rs2070197 polymorphism was identified as risk factors for SLE... | The meta-analysis confirms the association of IRF5 polymorphism with SLE in multiple populations. |
| PMID:23251221 | SUPPORT | Interferon regulatory factor 5 (IRF5) is a transcription factor which... genetic variants of IRF5 have been strongly linked to SLE pathogenesis. | The paper discusses the role of IRF5 in SLE pathogenesis and confirms its genetic association with the disease. |
| PMID:20453440 | SUPPORT | Recent large-scale studies in the Caucasian populations identified many new susceptibility genes to systemic lupus erythematosus (SLE)... In IRF5, the risk haplotype in Caucasians was not present in Japanese... All of these genes were associated with SLE... | The study confirms that IRF5 is associated with SLE in both Caucasian and Japanese populations. |
| PMID:36245280 | SUPPORT | IRF5 plays a crucial role in the development of lupus... Genome-wide association studies have identified several systemic lupus erythematosus (SLE) risk single-nucleotide polymorphisms (SNPs) enriched in the IRF5 locus. | The study identifies IRF5 as playing a key role in SLE development with confirmed risk SNPs. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:24763542 | SUPPORT | While it is known that UV radiation exposure may exacerbate pre-existing lupus, it remains unclear whether UV exposure is a risk factor for the development of SLE. | The literature clearly states that UV radiation exposure may exacerbate pre-existing lupus, which supports the statement. |
| PMID:22385883 | SUPPORT | Exposure to sunlight is one of the environmental factors involved in the pathogenesis of systemic lupus erythematosus. | The study investigates the seasonal variation in lupus flares and correlates increased flares with increased temperature and sunshine, supporting the statement that UV exposure exacerbates disease activity. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:36332998 | SUPPORT | This review focuses on SLE risk potentially associated with environmental factors including infections. | The paper identifies infections as one of the environmental factors potentially associated with the risk of SLE, thereby supporting the statement that infections can trigger or worsen disease symptoms in SLE. |
| PMID:25022358 | SUPPORT | New mechanisms for autoimmunity triggered by Epstein-Barr virus and human commensal microbiota have been described. | This review mentions infections, specifically Epstein-Barr virus, as triggers for autoimmunity, which supports the notion that infections can influence SLE disease activity. |
| PMID:38146370 | SUPPORT | The relationship between Systemic lupus erythematosus (SLE) and Epstein-Barr virus (EBV) infection has been suggested for decades, but the underlying mechanism of the EBV influence on SLE development remains to be elucidated. | This study supports the connection between infections (specifically EBV) and SLE, further establishing that infections can trigger or worsen SLE symptoms. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:25216337 | SUPPORT | It is currently believed that the onset of SLE and lupus flares are triggered by various environmental factors in genetically susceptible individuals… infections, sex hormones and certain medications and vaccines, have been implicated to induce SLE onset or flares... | This reference discusses various environmental factors that can trigger SLE flares, which supports the notion that stress, as an environmental factor, can do so as well. |
| PMID:36537191 | SUPPORT | In a racially diverse sample of individuals with SLE, those who experienced an increase in stress had significantly worse disease activity and greater symptom burden at follow-up compared to those with stress levels that remained stable or declined. | This reference directly supports the statement that psychological stress can trigger and worsen SLE flares. |
| PMID:36535611 | SUPPORT | Systemic lupus erythematosus (SLE) is a heterogeneous, multisystem autoimmune disorder characterized by unpredictable disease flares.... suggesting that stress-related disorders alter the susceptibility to SLE. | This reference indicates a link between stress-related disorders and the development or worsening of SLE. |
| species | genotype | background | genes | alleles | description |
|---|---|---|---|---|---|
| Mouse | MRL/lpr strain | None |
|
FAS lpr
|
genetically prone to develop lupus-like symptoms and APS |
| Mouse | None | (NZB/BlNJ x NZW/LacJ)F1/J | None | None | None |