Birgitta Gullstrand
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- 2009
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Mark
C1q inhibits immune complex induced IFN-alpha production in plasmacytoid dendritic cells-A novel link between C1q deficiency and SLE pathogenesis
(2009) 12th European Meeting on Complement in Human Disease In Molecular Immunology 46(14). p.2857-2857
- Contribution to journal › Published meeting abstract
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Mark
Influence of IgG allotypes on defense against Haemophilus influenzae type b in children-A complement-dependent mechanism?
(2009) 12th European Meeting on Complement in Human Disease In Molecular Immunology 46(14). p.2867-2868
- Contribution to journal › Published meeting abstract
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Mark
Complement classical pathway components are all important in clearance of apoptotic and secondary necrotic cells.
- Contribution to journal › Article
- 2008
-
Mark
SLE serum induces classical caspase-dependent apoptosis independent of death receptors
- Contribution to journal › Article
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Mark
Complement classical pathway components are all important in clearance of apoptotic cells
- Contribution to journal › Published meeting abstract
-
Mark
Role of C1q in regulation of IFN-alpha production
(2008) 72nd Annual Scientific Meeting of the American-College-of-Rheumatology/43rd Annual Scientific Meeting of the Association-of-Rheumatology-Health-Professionals In Arthritis and Rheumatism 58(9). p.706-706
- Contribution to journal › Published meeting abstract
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Mark
Serum bactericidal activity against Neisseria meningitidis in patients with C3 nephritic factors is dependent on IgG allotypes.
- Contribution to journal › Article
- 2007
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Mark
Genetically determined mannan-binding lectin deficiency is of minor importance in determining susceptibility to severe infections and vascular organ damage in systemic lupus erythematosus.
- Contribution to journal › Article
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Mark
Association between SLE nephritis and polymorphic variants of the CRP and Fc gamma RIIIa genes
- Contribution to journal › Article
- 2004
-
Mark
Induction of apoptosis in monocytes and lymphocytes by serum from patients with systemic lupus erythematosus - an additional mechanism to increased autoantigen load?
- Contribution to journal › Article