Complement Cascade (Bowden) Flashcards
C’ functions
triggering amplification of inflammation reactions
attracting phagocytes by chemotaxis
clearance of immune complexes
cellular activation
direct microbial killins
important development of humoral responses
Anaphylatoxins
the a fragments from C’ cascade. play a role in initiating localized inflammatory response
C’ role in classical pathway
activated by Ab binding to Ag
viruses and bacteria.
assists Ab and adaptive immune system
C’ role in alternative pathway
independent of Ab. Innate immunity
always on guard.- surveillance
Which C’ pathway is most rapid and efficient
Classical
How can we distinguish self membrane from non-self
self: high [ ] sialic acid & rapidly inactivates bound C3b via Factor H
non: low [ ] sialic acid & bound C3b remains active longer, ex: bact/yeast walla and viral envelopes
Two main types of Regulation in C’ cascade
proteolytic digestion
binding with dissociation
What acts as opsonin, what R do they bind to
C3b and C4b
these bind to CR1,-CR4 on phagocytes
What else activates phagocytic cells
C5a anaphylatoxin thru
increase # C’R on cell surface
What removes immune complexes with C3b
monocytes and phagocytes–>liver
erythroctyes–>spleen
How many MACs does it take to lyse RBC
1
What type of cells are resistant to MACs
nucleated. can endocytose MACs because they are repairing membrane damage
some cancer cells have this ability
Activation of complement results in what direction of fluid flow
influx of fluid
Fucntions of anaphylatoxins
bind R of mast cells and blood basophils to induce degranulation
induce sm. mm contraction to inc vascular perm
induce monocytes and neutrophils to adhere endothelial cells–>extravasation
Which C’ a fragment is the most potent
C5a
Prokinin
C2a cleaved by plasmin to yield kinin–> EDEMA
What are they general schemes of many complement particle pathways to degradation
Opsonization of C3b or C4b and phagocytosed
Complement mediated- MAC formation= osmotic lysis
Stimulation of inflammatory rxns via a fragments(destruction is by leukocytes)
C3 deficiencies
life-threatening. severe recurrent infections right after birth.
C3b plays in opsonin of infectious material
What types of deficiencies mimic C3 deficiency
Facto H and I because unregulated C3b generation exhausts C3 from serum
MAC deficiencies
generally healthy
increase in infection by neisseria gonorrhoeae and N. meningitidis
Most common early C’ deficiency
C2 deficiency: high degree of systemic lupus erythematosis. inability to clear immune complexes.
this activates alternative pathways and leads to local inflammation
may promote breakdown of self antigens–>autoimmunity
C1 inhibitory deficiency
C1 not regulated. C4 and C2 levels are low
experience Hereditary Angioneurotic edema
Hereditaty Angioneurotic edema symptoms and Tx
attacks of swelling, no obvious cause. extremities, face and GI tract. upper respiratory tract
Tx: androgens to produce C1inhibitor
DAF deficiency
Paroxysmal Nocturnal Hemoglobinuria
acquired hemolytic disorder with spontaneous episodes of RBC lysis
Increased sensitivity to lysis
Treat with EPO
Epstein-Barr virus (herpesviridae)
uses CR2 as a R for attachment
Measles virus (paramyxovirdidae)
uses MCP(CD46) as R
The west nile virus (flavivirdae)
C3b coats viral particle and then gains entry into cell via the CR3 Receptor
