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antibody immune complexesmay triggercomplement activation
immune complexes ... antigenresultsin complement activation
The resulting immune complexescould triggercomplement activation
the presence of immune complexes(passive) triggered bycomplement system activation
immune complexes ( ICleadingto complement activation
that immune complexes can be formed in the microvasculature of the brain ,resultingin complement activation
PubMed ] Kuraya M , Ming Z , Liu X , Matsushita M , Fujita T. Specific binding of L - ficolin and H - ficolin to apoptotic cellsleadsto complement activation
antibody - antigen interactionsresultingin complement activation
/ FREE Full Text Kuraya M , Ming Z , Liu X , Matsushita M , Fujita T. Specific binding of L - ficolin and H - ficolin to apoptotic cellsleadsto complement activation
immunogenic immune complexes ... anti - eTG IgAtriggercomplement activation
Immune complexes as well as autoantibodies bound to antigens on cellscausecomplement activation
This antibody - antigen interactioncan causecomplement activation
Biomaterial Surfaces 1(passive) Triggered byComplement Activation
The initial factorscontributingto complement activation
chemotactic factorsresultingfrom complement activation
circulating immune complexes , which eventually become embedded on blood vessel wallstriggeringcomplement activation
chondroitin sulfate released by thrombin receptor - activated platelets 2008(passive) triggered byComplement activation
just a few antibody : antigen reactions(passive) can be triggered byComplement activation
Antigen / antibody complexmay leadto Complement activation
Antibody - antigen complexescausecomplement activation
biomaterial surfaces in contact with blood(passive) triggered bycomplement activation
pemphigus antibody characteristic inflammatory changes occurred(passive) caused bycomplement activation
The plasma was supplemented with EDTAto preventcomplement activation
Kuraya , M et al ; Specific binding of L - ficolin and H - ficolin to apoptotic cellsleadsto complement activation
endotoxin ... the many factors in hemoglobin preparationcan causecomplement activation
Binding of antibodies to proteinsleadsto complement activation
Self - reactive antibodycausesactivation of complement
the antibody titer ... too lowto causecomplement activation
the antibody titre ... too lowto causecomplement activation
chondroitin sulfate released by thrombin receptor - activated platelets J Thromb Haemost(passive) triggered byComplement activation
Immune complexes , surface components of bacteria and yeast , C - reactive protein , mitochondria and necrotic cellstriggercomplement activation pathways
Biomaterial Surfaces Mechanisms and Regulation 5(passive) Triggered byComplement Activation
Biomaterial Surfaces Mechanisms and Regulation 4(passive) Triggered byComplement Activation
Biomaterial Surfaces Mechanisms and Regulation Author(passive) Triggered byComplement Activation
Biomaterial Surfaces Mechanisms and Regulation Författare(passive) Triggered byComplement Activation
hemolytic - uremic syndrome ’ Eculizumab ... a monoclonal antibodypreventscomplement activation
the tumor cells without antibody(passive) caused bycomplement activation
This natural antibody will then recruit C1qleadingto complement activation
intragraft MCMV - specific IgG antibody depositionleadingto complement activation
chondroitin sulfate released by thrombin receptor - activated platelets chondroitin sulfate , coagulation , complement , platelets(passive) triggered byComplement activation
tissue damage ( Clarkcausingtissue damage ( Clark
in significant tissue damagecan resultin significant tissue damage
cell lysis , inflammation or damage by macrophagescausescell lysis , inflammation or damage by macrophages
to local and remote tissue damageleadingto local and remote tissue damage
to remote tissue damage after mesenteric IRcan leadto remote tissue damage after mesenteric IR
Intravascular hemolysis of erythrocytes in IMHA(passive) is caused byIntravascular hemolysis of erythrocytes in IMHA
extensive tissue damage through the mediators of inflammation producedmay causeextensive tissue damage through the mediators of inflammation produced
to this progressive kidney injury ( 108contributesto this progressive kidney injury ( 108
to robust and efficient proteolytic cascades , which terminate in opsonization and lysis of the pathogen as well as in the generation of the classical inflammatory response through the production of potent proinflammatory moleculesleadsto robust and efficient proteolytic cascades , which terminate in opsonization and lysis of the pathogen as well as in the generation of the classical inflammatory response through the production of potent proinflammatory molecules
to cell lysis , which is effectuated by MACcan leadto cell lysis , which is effectuated by MAC
to intravascular hemolysis and an inflammatory prothrombotic stateleadingto intravascular hemolysis and an inflammatory prothrombotic state
to formation of the membrane attack complex ( MAC ) , known to assemble on retinal pigment epithelial ( RPE ) cellsleadsto formation of the membrane attack complex ( MAC ) , known to assemble on retinal pigment epithelial ( RPE ) cells
to progressive kidney damage and failurecan leadto progressive kidney damage and failure
in red blood cell lysisresultsin red blood cell lysis
to inflammation resulting in tissue injury of multiple organsleadsto inflammation resulting in tissue injury of multiple organs
to cell lysis ( complement - dependent cytotoxicity [ CDCultimately leadingto cell lysis ( complement - dependent cytotoxicity [ CDC
to systemic inflammation and migration of neutrophils to the lungs ... perpetuating tissue damage [ 69contributeto systemic inflammation and migration of neutrophils to the lungs ... perpetuating tissue damage [ 69
self - tissue injury ... leading to pathologic conditionsmay triggerself - tissue injury ... leading to pathologic conditions
to leukocyte recruitment and neuropathic pain following peripheral nerve injury in ratscontributesto leukocyte recruitment and neuropathic pain following peripheral nerve injury in rats
to membrane attack complex ( MAC ) formationleadingto membrane attack complex ( MAC ) formation
Full description Background Atypical haemolytic uraemic syndrome ( aHUS(passive) is caused byFull description Background Atypical haemolytic uraemic syndrome ( aHUS
to vascular injuryfurther contributesto vascular injury
to all of these forms of injurymay contributeto all of these forms of injury
cellular injury(passive) caused bycellular injury
to jejunal injuryleadingto jejunal injury
to hypoxic - ischemic brain injury in neonatal ratscontributesto hypoxic - ischemic brain injury in neonatal rats
the generation of cleavage products , including the anaphylatoxins C3a and C5a ( 5triggersthe generation of cleavage products , including the anaphylatoxins C3a and C5a ( 5
damage to host cells alsocan causedamage to host cells also
chemotaxis , cell adherence , cell lysis , phagocytosis , and mast cell activationcauseschemotaxis , cell adherence , cell lysis , phagocytosis , and mast cell activation
to podocyte damage inmay contributeto podocyte damage in
to fetal damageleadingto fetal damage
to both glomerular and tubulointerstitial damage in adriamycin nephropathy in micecontributesto both glomerular and tubulointerstitial damage in adriamycin nephropathy in mice
to C3 deposition and MAC formation on the cell surfaceleadingto C3 deposition and MAC formation on the cell surface
in immune adherence and phagocytosis , local inflammation and cell lysiscan resultin immune adherence and phagocytosis , local inflammation and cell lysis
to glomerular and tubular injury in experimental FSGScontributesto glomerular and tubular injury in experimental FSGS
to glomerular injury and sclerosis in some patients with FSGScontributesto glomerular injury and sclerosis in some patients with FSGS
in significant increase of C4a split productresultingin significant increase of C4a split product
to angiogenesis with the formation of new blood vesselsleadingto angiogenesis with the formation of new blood vessels
to tissue injury and perpetuation of inflammatory response ( Peerschke et al . , 2004may contributeto tissue injury and perpetuation of inflammatory response ( Peerschke et al . , 2004
to the pathogenesis of vascular leakage that occurs in patients with DHF / DSS [ 26may contributeto the pathogenesis of vascular leakage that occurs in patients with DHF / DSS [ 26