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complement team-based learning
Terms in this set (19)
1. C1q, which binds to the Fc region of pathogen-bound antibody,
2. C1r, a protease that is activated when C1q binds to antibody
3. C1s, a protease that is activated by C1r.
which three proteins make up the C1 complex
it needs to bind to either 1 IgM or at least 2 IgG on the surface of pathogens
what does the C1 complex need to bind to during the classical pathway of complement activation
C3d-tagged antigens can be retained by antigen-presenting cells called follicular dendritic cells for recognition by antigen-specific B cell
how does complement play a role in recognition by antigen-specific B cells
it enhances BCR signaling, which amplifies B Cell Activation, proliferation, and differentiation into antibody secreting cells
what happens when CR2 receptors on the surface of B cells come in contact and recognize C3D molecules attached to antigen
they have very short half-life when not bound to microbial surfaces
describe the half-life of soluble complement
it is an important soluble regulator of the classical pathway. it inactivates the protease activity of C1. activation of the classical pathway precedes past this point by generating sufficient C1 to overwhelm the inhibitor
what is the C1 inhibitor
it is a Cell Wall anchored protein of staphylococcal Aureus that binds to the FC portion of IgG. this prevents FC receptor-mediated phagocytosis and also blocks C1q binding to IgG.
how does staphylococcal protein A reduce antibody mediated phagocytosis and activation of the classical complement pathway
streptococcus pyogenes (surface exposed M proteins bind C4BP) and neisseria gonorrhea (which binds C4 BP on its outer membrane porin and pili)
what are two examples of bacteria that can recruit soluble negative Regulators of C3 and C3 products
These structures include factor H binding protein expressed on the surface of
, porin expressed on the surface of
, and M1 protein and Hic (factor H binding inhibitor of complement) expressed on Streptococcus pneumoniae.
name some bacteria that have the ability to bind Factor H, which facilitates the rapid decay if C3 convertases
by promoting the recruitment of Factor H. B N. meningitidis, Escherichia coli K1, and Streptococcus agalactiae are examples.
How does Sialic acid slow down the activation of complement
One, sialic acid is negatively charged, which limits phagocytic uptake by neutrophils and macrophages. Two, the addition of sialic acid is a form of "molecular mimicry," since human glycoproteins such as neural cell adhesion molecule (NCAM) are also sialylated and, therefore, mimic self proteins and are not recognized by antibodies.
What are two other benefits of Sialic acid aside from slowing down the activation of Complement
Gram-positive bacteria (e.g. Streptococci, Staphylococci)
Which type of bacteria possess thick cell walls and are intrinsically resistant to direct lysis by membrane attack complex (MAC) formation.
thick polysaccharide capsules
What do some Gram-negatives (including N. meningitidis, Hemophilus influenzae, and Klebsiella pneumoniae) have that limit lysis by MAC.
recurrent, life-threatening infections with pyogenic bacteria, particularly Haemophilus influenzae, Streptococcus pneumoniae, and Staphylococcus aureus. Inheritance is autosomal recessive
What is the consequence of C3 deficiency
These deficiencies fail to form the membrane attack complex and, thus, lead to a significant incidence (7,000-10,000 fold higher risk) of infection with Neisseria sp. (causing meningitis and gonorrhea). Also, C5 deficient patients also lack the ability to mount an efficient chemotactic response because the generation of C5a is significantly impaired
What are some consequences of Deficiencies in late complement components (e.g. C5-C9).
Infections with pyogenic bacteria and/or Neisseria are not increased, since the alternative pathway of complement activation can still be used. However, there is a significant incidence of systemic lupus erythematosus and glomerulonephritis. These conditions are thought to result from a failure to clear immune complexes as well as cellular debris, which then leads to the development of autoantibodies and circulating immune complexes that can be deposited in the kidney.
What is the consequence of deficiencies in C1, C4, and C2 (classical pathway activation sequence)
Partial C4 deficiency
What is the most common complement deficiency in humans (~30%).
paroxysmal nocturnal hemoglobinuria
What disease is linked with deficiencies in DAF and CD59 (failure to prevent the formation of the MAC on their cells)
CH50 (total hemolytic complement) Test
This test is used to determine the efficiency of activating the classical pathway by measuring lysis of antibody-coated red blood cells by serum from an individual suspected of immune deficiency.
What test is used to measure both the serum levels and the activity of complement components C1q/r/s, C4, C2, C3, C5, and C6-C9.
Recommended textbook explanations
Lehninger Principles of Biochemistry
David L Nelson, Michael M. Cox
Miller and Levine Biology
Joseph S. Levine, Kenneth R. Miller
Fundamentals of Biochemistry: Life at the Molecular Level
Charlotte W. Pratt, Donald Voet, Judith G. Voet
Campbell Biology (AP Edition)
Cain, Campbell, Minorsky, Reece, Urry, Wasserman
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