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SLE - Coggle Diagram
SLE
Autoantibodies
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Anti-Smith (Sm) antibodies (Antigen sind Proteinbestandteile der snRNPs (Komplexe aus RNA und Protein), die das Spliceosom bilden) -> most specific for SLE
specificity for RNA-binding proteins (Ro, La, Sm and RNP)
Epidemiology
US: incidence 2-7.6/100,00, prevalence 19-159/100,000
Europe: incidence 1-4.9/100,000, prevalence 28-97/100,000
More common in women than in men -> mainly woman in childbearing age -> female/male is 3/1 in children and 9/1 in childbearing age
More common in certain racial and ethnic groups: Higher in people of African origin, native Americans, Indigenous Australians ahd people of Chinese background
Meta-analysis: Mortality ratio of 3 -> varies due to ethnicities, low socioeconomic
background, availibility of treatment, infections, involved organ system (highest with nephritis)
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Genetic factors
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more than 100 genetic loci with small effect on risk -> aggregation of genetic risks might achieve a threshold
Many genetic variants are regulatory elements -> invilved in important molecular pathways altering immune function
Organ damage
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a differentiated monocyte population mediating uncontrolled tissue repair -> contributes to scleoris and organ dysfunction
Lupus nephritis
Immune complexes are deposited in glomerulus -> complement activation and recruitment og myeloid cells
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treatment
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Immunosuppressants
Tacrolimus, voclosporin (calcineurin inhibitor)
glucocorticoids (often as initial therapy), e.g. prednisolone
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Environmental factors
Viral infections: EBV -> contribute to innate immune system activation, production of Abs specific for amino acid sequences shared by self-proteins and EBV-proteins (e.g. EBNA1 and dsDNA)
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