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no wayto preventcomplement deficiencies
their particular mutation(passive) caused bycomplement deficiencies
unrestricted complement activitycausingcomplement deficiency
It is important from birthto preventautodegradation of complement deficiency
PNH ... the PIG - A generesultsin deficiency of complement
Polymorphism in ficolin-3 gene ( FCN3can leadto complement deficiency
a novel mutationleadingto a complement deficiency
molecular mechanismsleadingto complement deficiency
no proven strategiesto preventautodegradation of complement deficiency
in immunologists(passive) was discoveredComplement deficiency
life - threatening diseasesoccasionally causelife - threatening diseases
severe recurrent bacterial and fungal infections in the bodycan causesevere recurrent bacterial and fungal infections in the body
to the autoimmune disease , systemic lupus erythematosus ( SLEcontributesto the autoimmune disease , systemic lupus erythematosus ( SLE
symptoms like allergic reactions ( hives , rashes , swelling ... and it is possible the complement deficiency can also create lupuscan createsymptoms like allergic reactions ( hives , rashes , swelling ... and it is possible the complement deficiency can also create lupus
in an increased susceptibility to disease ( 5 pointscan resultin an increased susceptibility to disease ( 5 points
someone with Lupus(passive) caused bysomeone with Lupus
to susceptibility to infectionleadsto susceptibility to infection
to recurrent bacterial infectionsleadto recurrent bacterial infections
to life - threatening infections as well as long term autoimmune conditions and organ injuriescan leadto life - threatening infections as well as long term autoimmune conditions and organ injuries
in infections caused by encapsulated pyogenic bacteria , especially Neisseria speciesresultin infections caused by encapsulated pyogenic bacteria , especially Neisseria species
SLE by impairment of the physiological clearance of apoptotic cells by macrophagescausesSLE by impairment of the physiological clearance of apoptotic cells by macrophages
SLE ... and yet SLE causes activation and consumption of complementcausesSLE ... and yet SLE causes activation and consumption of complement
lupus is hard to reconcile with the concept that complement activation products are the major cause of inflammatory injury in the diseasecauseslupus is hard to reconcile with the concept that complement activation products are the major cause of inflammatory injury in the disease
clinical problems that are dictated by the part of the system affectedcauseclinical problems that are dictated by the part of the system affected
in a wide variety of clinical spectrum.3resultin a wide variety of clinical spectrum.3
in defective clearance of immune complexes and apoptotic cells and failure of B cell tolerancemay resultin defective clearance of immune complexes and apoptotic cells and failure of B cell tolerance
to impaired handling of immune complex and inadequate clearance apoptotic cell debris [ 11 , 12leadsto impaired handling of immune complex and inadequate clearance apoptotic cell debris [ 11 , 12
to autoimmunity by altering processing of antigen - antibody complexes and/or activation of Fc receptorscontributeto autoimmunity by altering processing of antigen - antibody complexes and/or activation of Fc receptors
from genetic mutationsresultingfrom genetic mutations
impaired clearance of these immune complexeslikewise causesimpaired clearance of these immune complexes
to increased apoptosis , which leads to a decrease in the presence of self - antigens , thus altering peripheral toleranceleadsto increased apoptosis , which leads to a decrease in the presence of self - antigens , thus altering peripheral tolerance
incomplete maintenance of peripheral tolerancecausesincomplete maintenance of peripheral tolerance
to an inability to clear circulating immune complexesleadsto an inability to clear circulating immune complexes
bacteria to not be opsonizedwould causebacteria to not be opsonized
from the lack of C1 esterase inhibitorresultingfrom the lack of C1 esterase inhibitor
to poor host resistance against candidiasisleadsto poor host resistance against candidiasis
to impairment of apoptotic clearance causing a potent source of auto - antigencan also leadto impairment of apoptotic clearance causing a potent source of auto - antigen
to a breach in self - toleranceleadsto a breach in self - tolerance
to a decrease in the formation of antibody - antigen - complement immune complexesleadsto a decrease in the formation of antibody - antigen - complement immune complexes
in overactive complement , which causes vasodilation+vasopermeabilityresultsin overactive complement , which causes vasodilation+vasopermeability
in accumulation of functional autoreactive cells ... possibly leading to autoimmunitycould resultin accumulation of functional autoreactive cells ... possibly leading to autoimmunity
to an increase in inflammatory monocytes , which leads to a chronic inflammatory stateleadsto an increase in inflammatory monocytes , which leads to a chronic inflammatory state
the formation of atherosclerotic lesions.3preventsthe formation of atherosclerotic lesions.3
to decreased binding to self - antigens from apoptotic cells , resulting in an increased amount of self - antigen present , thus increasing the chances of encountering autoreactive lymphocytesleadsto decreased binding to self - antigens from apoptotic cells , resulting in an increased amount of self - antigen present , thus increasing the chances of encountering autoreactive lymphocytes
to increased killing of regulatory T cells , which allow autoreactive lymphocytes to escape apoptosisleadsto increased killing of regulatory T cells , which allow autoreactive lymphocytes to escape apoptosis
dendritic atrophy in DBA/2 J glaucomapreventsdendritic atrophy in DBA/2 J glaucoma
to autoimmune disorders and impairs tissue regenerationleadsto autoimmune disorders and impairs tissue regeneration
the early pro - apoptotic and pro - inflammatory effects of complement mediated by the anaphylatoxins and opsonins that trigger complement - dependent phagocytosis , an effect that is also achieved by complement inhibitionwill preventthe early pro - apoptotic and pro - inflammatory effects of complement mediated by the anaphylatoxins and opsonins that trigger complement - dependent phagocytosis , an effect that is also achieved by complement inhibition
to renal vasoconstrictionleadingto renal vasoconstriction
immune complex diseases(passive) caused byimmune complex diseases