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158 Cards in this Set
- Front
- Back
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Circulating native/mature B cell can be activated by _____.
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repetitive epitopes on a bacteria cell wall.
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The initial signal pathway by Igα:β. (2 steps)
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1. ITAMs physphorylated by BLK, Fyn, Lyn.
2. Syk bind to doubly phosphorylated β chain |
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ITAMs are phosphorylated by what three molecules?
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Blk, Fyn, Lyn
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What three co-receptor molecules are associated with B cell activation?
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1. CD21(CR2): complement receptor 2
2. CD19: signaling chain 3. CD81 (TAPA-1) |
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What's the function of CD21?
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complement receptor 2: binds to complement fragments C3d, iC3b, C3dg.
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Where is CR2 located and what's its function?
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part of B cell coreceptor and it binds to complement fragments C3d, iC3b, C3dg.
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What type of antigens can activate B cells without T cell's help?
What are these antigens called? |
repetitive epitopes on bacterial cell walls and capsules.
thymus-independent antigen (TI-antigen) |
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What are the two categories of TI antigens?
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TI-1: bind to both BCR and other recoptors (eg.LPS: bind to CD14 and TLR)
TI-2: repetitive epitopes in high concentration |
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What's the difference in antibodies produced in B cells activated by TI-1 and TI-2?
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TI-1 produces antibodies not only specific for the this antigen, but also others present on the microorganism.
TI-2: only produce antibodies specific for that one antigen |
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What's one limitation of the early antibody response cause by TI-2 antigens?
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There is little isotype switching and somatic hypermutation. Predominantly IgM.
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What's the function of CD19?
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Signal transduction synergistic with Igα:β.
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Which of the following phosphorylated the cytoplasmuic tail of CD19?
A. Blk B. Fyn C. Lyn |
C.
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TD antigens need CD4 T cells to activate B cells. What molecule specifically on the the T cell that binds to another recoptor on the B cell?
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CD40L
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B cell receptor consists of:
A. CD1 and CD19 B. CR2(CD21), CD19, TAPA-1(CD81) C. Igα:β and membrane Ig molecules D. ITAMs, VCAM-1, membrane Igs E. TCR, CD3, membrane Igs |
B.
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Do TI-1 and 2 antigens generate memory cells?
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No.
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Which of the following does not generate antibody response in infants?
A. TD antigen B. TI-1 antigen C. TI-2 antigen |
C.
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Which of the following stimulate nonspecific B cells?
A. TD antigen B. TI-1 antigen C. TI-2 antigen |
B.
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Which of the following generate long term memory B cells?
A. TD antigen B. TI-1 antigen |
A.
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T/F: HyperIgM syndrome is an immunodeficiency characterized by a lack of CD40 ligand expression on T cells.
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T.
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T/F: Plasma cells produces secreted antibody, proliferate and undergo somatic hypermutation to produce antibodies with higher affinity for antigen.
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F.
B cells proliferate and undergo somatic hypermutation to produce antibodies with higher affinity for antigen and differentiate into the endstage differentiated plasma cell, plasma cells produce secreted antibodies. |
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T/F: TI-2 polysaccharide antigens are commonly used in vaccines for infants because they stimulate strong antibody response.
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F.
TI-2 antigens activate only mature B cells. Usually B1 cells that usually don't mature until age 5. Need to conjugate with TD antigens inorder to build memory cells. |
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T/F: Antibody-dependent cell-mediated cytoxicity is mediated by NK cells which bind to antibody-coated target cells using Fc receptors and kill target through apoptosis.
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T.
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In Hib vaccine, why is H. influenzae conjugates to either Diptheria or tetnus toxoid?
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Diptheria and tetnus toxoid are TD antigens which will build memory cells which H. influenzae can't since it's a TI antigen.
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Diptheria and tetnus are:
A. TD antigens B. TI-1 antigens C. TI-2 antigens |
A.
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A feature not associated with B1 cell:
A. bind bacterial polysaccaride capsules B. high affinity IgG synthesis C. IgM production D. limited set of V-regions E. self-renewing |
B.
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Steps of signal transduction leading to primary focus presence in the T-cell area.(4)
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1. CD40L of T cell bind to C40 on B cell
2. transcription factor NFκB to express ICAM1 3. T cell activated to produce cytokine IL4(Th2) 4. IL4 activate B cell proliferation and differentiation. |
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What ILs from Th2 stimulate B cell to become plasma cells in the medullary cords?
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IL5,6
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An individual lacking the gene for CD40L would:
A. be deficient in CD8 T cells. B. be resistant to Epstein-Barr virus. C. lack the ability to switch isotypes. D. make only IgG response to polysaccharide antigens. E. produce high levels of oponins. |
C.
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How would an immune complex containing IgM bind to FDCs?
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IgM fix complement which can bind to CR2 of FDC.
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The dark zone of the germinal center is populated with____:
A. mature B cells B. centroblasts C. centrocytes D. resting B cells |
B.
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The light zone of the germinal center is populated with____:
A. FDCs B. centrocytes C. A and B D. resting B cells |
C.
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The mantle zone of the germinal center is populated with____:
A. nonspecific B cells B. centroblasts C. centrocytes D. resting B cells |
A.
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Somatic hypermutation happens during ____.
A. centroblast B. centrocyte C. Both |
C
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Two competition events for centrocytes to survive:
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1. compete for access of antigen on FDC
2. compete for antigen specific T helper cell. |
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What are immune complexes?
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antibody-antigen, or antibody-complement-antigen
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FDC has receptors for the Fc region of Ig__, and for complement__.
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IgG, C3b
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Are immune complex on FDC internalized?
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No
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What are iccosomes?
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immune-complex coated bodies that bud off from FDC.
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Does FDC have MHCIIs?
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No. They are not bone marrow derived.
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What series of events happens after centroblasts proliferate into centrocytes in order to survive? (4)
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1. centrocytes move to L zone to contact FDC.
2. capture antigen or iccosomes, present anigen on MHCII. 3. centrocytes move to peripheral T cell area: engagement of CD40 to Th2 CD40L 4. centrocytes activated to undergo isotype switch and express Bcl-x1 protein which prevents apoptosis. |
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Purposes of interaction of a mutated centrocyte and a T cell. (2)
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1. proliferation of both B and T cells.
2. anergy of self-reactive centrocytes |
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What are tingible body macrophages?
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macrophages that have recently engulfed apoptotic centrocytes.
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How would an immune complex containing IgM bind to FDCs?
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IgM will fix complement which can bind to CR2 of FDC.
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How would an immune complex containing IgG bind to FDCs?
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FDC has Fc receptor for IgG, but not IgM.
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Why FcγR and complement receptors are not phagocytosed bt receptor mediated endocytosis observed by macrophages?
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FDCs has no MHCII to present antigens if immune complex is internalized.
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The site of affinity maturation of B cells in germinal centers:
A. follicular dendritic cells B. interdigitating dendritic cells C. Langerhans cells D. macrophages E. plasma cells |
A.
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IL-4 made by Th2 cells would induce isotype switch from IgM to ___.
A. IgG1 B. IgA C. IgE D. IgG1 and IgE |
D.
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IL-5 made by Th2 cells would induce isotype switch from IgM to ___.
A. IgG1 B. IgA C. IgE D. IgG1 and IgE |
B. (augments production)
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TGF-β made by Th2 cells would induce isotype switch from IgM to ___.
A. IgG1 B. IgA C. IgE D. IgG2 and IgA |
D.
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Th2 cytokines IL-4, IL-5, and TGF-β will activate B cells to secrete IgM and class switch IgM into what other Igs?
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IgA, IgE, IgG2, IgG4 (IgG2, IgG4 are weak opsonizers)
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Th1 cytokine IFN-γ will induce B cell to class switch IgM to ____.
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IgG1 (strong opsonizer)
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What is the function of CD45 in B cells?
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Allows activation of receptor associated kinases:Blk, Fyn, and Lyn.
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What are the two funcitons of Fc region of antibodies?
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1. deliver antibody to anatomical sites for another protein and cells of the immune system.
2. link bound antigen to molecules or cells that will effect its destruction. |
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Why is IgM efficient in poreventing blood borne infections?
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Its pentameric structure binds well with carbohydrates, lipid, and protein antigens in the blood and the large complex cannot then cross vascular wall to the tissues.
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IgM can bind to what kind(s) of antigen(s)?
A. TI antigens B. TD antigens C. both |
C.
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Why is IgM so efficient in fixing complement?
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A single IgM pentamer can activate complement where as at least 2 IgGs are needed to activate C1qrs.
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Why is IgM not efficient in engaging phagocytosis of immune complexes?
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There is no Fc receptor for IgM. Unless complement has been activated by IgM and C3b has been deposited on the pathogen surface, then the IgM:antigen:C3b complex can be taken up by macrophage after binding to the complement receptor.
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What is septicemia?
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Blood-borne infection.
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Which two antobodies are effective in preventing septicemia?
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IgM, IgG
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Where do you find dimeric IgA?
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secondary lymph tissue underlying mucosa.
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How does dimeric IgA cross epithelial barrier?
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Dimeric IgA is transported by poly-Ig receptor on the basolateral surface of epithelial cells.
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After dimeric IgA transcytosed to the mucosal side, it is bound to ____ of poly Ig.
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Secretory component
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How does IgG cross epithelial barrier?
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Actively transported using Fc receptors called the Brambell receptor(FcRB) on endothelial cells.
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FcRB is structually similar to ___.
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MHC class I.
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How many FcRBs are needed for the transport of IgG?
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2
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Why does IgG have a relatively longer halflife?
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It is mainly located in extrecellular space, protected from the serum proteases.
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Where is IgA located in the body?
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Mucosal surfaces, eyes, nose, throat,mammary gland.
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Stimulation of the GALT results in produciton of IgA by:
A. activated macrophage B. activated B cells C. epithelial cells D. globlet cells E. M cells |
B.
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This molecule is transported by the poly-Ig receptor:
A. IgA B. Dimeric IgA C. monomeric IgM D. IgG E. IgE |
A.
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Final locations of transported IgG:(2)
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1. infected tissue
2. fetal circulation during pregancy |
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The maternal Ig isotype present in breast milk:
A. IgA B. IgD C. IgE D. IgG E. IgM |
A.
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When is the critical period for the newborn when there is a transient low IgG level?
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3 months- 1year
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What is a toxoid?
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Denatured toxin
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What is the main function of high affinity IgG and IgA?
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neutralization of microbial toxins and venoms.
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For A-B toxins such as diptheria and tetnus, which domain do IgG and IgA bind to neutralized the toxins?
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binding domain
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What's the best therapy for patients bitten by poisonous snakes?
What type of immunity is this? |
Infusion of antibodies specific for the venom (made by immunizing domestic animals).
Passive artificial immunity |
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As neutralizers, IgG and IgA prevent viral infection by binding to _____.
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protein on the outer envelope.
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As neutralizers, IgG and IgA prevent bacterial infection by binding to _____.
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Adhesion molecules (eg adhesin)
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As neutralizers, IgG and IgA prevent influenza by binding to _____ on the outer envelope.
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hemagglutinin
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As neutralizers, IgA prevent salmonella or Neisseria gonorrhea by binding to _____.
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Adhesin
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How do our body eliminate neutralized pathogens?
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neutophils, blood monocytes, tissue macrophages.
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How is Fcγ receptors different from FcRB of the endothelial cells?
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FcRB:
1. like MHCI (2 polypeptide chain αβ) 2. need 2 of these to bind to Fc 3. function in transport across endothelium. Fcγ receptors: 1. single polupeptide chain α 2. need 1 of these to bind to Fc 3. function in phagocytosis of neutralized pathogens |
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Which two Fcγ receptors are inhibitory?
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FcγRII-B1 and B2
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What's on the cytoplasmic tails of inhibitory Fcγ receptors that are involved in the signal transduction?
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ITIMs
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What poplypeptide chain is associated with signal transduction of Fcγ receptors?
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γ chain
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Why is stretococcus pneumoniae require anttobodies to coat before they are phagocytose?
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Cell-surface structures resistant to direct phagocytosis.
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What is the difference between IgG and IgE in binding with Fcγ receptors?
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IgG: low affinity binding when antigen is absent
IgE: high affinity even when antigen is absent |
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T/F: To activate a mast cell, the antigen must crosslink at least 2 IgEs and associated receptors.
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T
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What's on the cytoplasmic tails of inhibitory Fcγ receptors that are involved in the signal transduction?
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ITIMs
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What poplypeptide chain is associated with signal transduction of Fcγ receptors?
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γ chain
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Why is stretococcus pneumoniae require anttobodies to coat before they are phagocytose?
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Cell-surface structures resistant to direct phagocytosis.
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What is the difference between IgG and IgE in binding with Fcγ receptors?
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IgG: low affinity binding when antigen is absent
IgE: high affinity even when antigen is absent |
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T/F: To activate a mast cell, the antigen must crosslink at least 2 IgEs and associated receptors.
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T
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What is the 'natural' targets of IgE?
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parasites. Mast cell, eosinopjils and neutrophils are activated to degrannuate and kill parasites.
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How do macrophages kill parasites too big to phagocytose?
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release contents of lysosomes and poured to the parasite.
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What's the action of IgE activated granulocytes and mast cells to get rid of large parasites?
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Degranulation:
1. enzymes kill parasites. 2. inflammatory mediators cause smooth muscle contration of airway and gut to expel parasites 3. vaodilation flush out parasites. |
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What is antibody-dependent cell-mediated cytotoxicity (ADCC)?
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NK cells kill human cells coated by antibodies: require preformed antibodies.
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What are some similarities between FcεRI(mast cell) and FcγRIII(NK cell)?
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1. activation requires binding of antigen:antibody complexes to Fc receptors
2. release granules through exocytosis |
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What are some differences between FcεRI(mast cell) and FcγRIII(NK cell)?
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1. exocytosis of grannules in NK cell is polarized where as in mast cell is at random.
2. mast cells bind IgE whereas NK cells bind IgG. 3. IgE binds FcεRI in the absence of antigen 4. mast cell release mediators that affect other cells, NK cells release apoptosis-inducing compounds that kill taget cells directly. 5. ADCC by NK cell can be achieved in newborns by maternal IgG. |
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NK cells can induce apoptosis in target cells by ADCC using IgG and ____:
A. FcεRI B. FcγRI C. FcγRIII(CD16) |
C.
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What are the three complement activation pathway?
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1. Classic pathway
2. Lectin pathway 3. Alternative pathway. |
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Where are all complement components made?
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Liver
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T/F: Enzyme of the complement circulate in the blood in the active form.
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F. They are zymogens.
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Where does complement activation take place?
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Tissue
Blood |
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Which molecule is common to all three complement activation pathways?
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C3b
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What is complement fixation?
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When C3b is bound to the pathogen's surface.
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Differences in activation of the classical, lectin, and alternative complement pathways.
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1. Classical pathway: require IgM bound to LPS.
2. Lectin pathway: require mannose-binding protein inresponse to IL-1, IL6, TNF-α. 3. alternative pathway: require an activating surface of a pathogen which stablizes complement components. |
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Which of the three complement activation pathways is considered aquired and which is innate?
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aquired: classical
innate: lectin, alternative |
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Complement activation pathway(s) that funciton in innate response to infectious diseasedo not include:
A. Alternative pathway B. Lectin pathway C. Classical pathway |
C
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Mannose-binding lectin(MBL) and mannose-associated serum protein(MASP) are produced in the liver in response to what cytokines?
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IL-1, IL-6, TNFα.
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What is L-ficolin?
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a lectin pathway activator present in normal human plasma.
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How does L-ficolin activate the lectin pathway?
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Upon binding ligand, L-ficolin initiates C4 cleavage via MASP-2(mannose-associated serine protease)
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The mannose binding protein(MBP)is an acute-phase protein induced by:
A. C3a, C4a, C5a B. IFN-γ C. IL-1, IL-6, TNF-α D. IFN-γ, IL-12 E. IL-2, IL-4, IL-5 |
C.
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What are the three stages in the classical complement pathway?
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1. C1q bind to Fc region of Ig:antigen complex.
2. C1r activated: self cut, activate another and two C1s. 3. C1s cleaves C4 and C2: C4b covalently bind to pathogen surface (thioester bond), C2a bind to C4b. -> C3 cleavage. |
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What are the components on the classical C3 convertase? (2)
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C4b2a
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What are the components in the alternative C3 convertase?
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C3bBb
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What's the common enzymatic reaction referred to as the complement fixation?
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C3 cleaved into C3a and C3b, and C3b bind to pathogen surface using thioester bond.
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What are the effector functions of C3b? (2)
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1. binds and tags pathogen
2. contribute to C5 convertase. |
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What are the functions of C3a, C4a, and C5a?
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inflammatory mediators(ie. increase vascular permeability)
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Complement system peptide mediators of inflammation are:
A. C6, C7, C8 B. C1, C2, C4 C. C2b, C3b, C4b D. C3a, C4a, C5a E. Bb, D, C3b |
D.
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What is the function of α2-macroglobulin?
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protease inhibitor of plasma: has thioester bond property similar to C3, C4.
Inhibits thrombin and plasmin formation. |
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Systemic lupus erythematosus(SLE):
1. cause 2. symptom |
1.lack C4A
2. autoimmune: body produces antibodies which form complexes that are not cleared effectively. Damage to renal glomeruli because of high level of immune complexes. |
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C4 genes are located in which region of the MHC locus?
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MHCIII
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What's the difference between C4A and C4B (not C4a and C4b)?
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These are the two forms of C4.
C4A: thioester bond attacked by amino groups of macromolecules. C4B: thioester bond attacked by -OH groups. |
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Describe the process the alternative C3 convertase is formed.
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1. Factor B bind to C3b
2. Factor D cleaves factor B into Ba and Bb, Bb bound to C3b. 3. result in C3bBb |
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In addition to IgG, which complement component is a powerful opsonin?
A. C4b B. C3b C. C3a D. C5a E. C1q |
B.
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Which of the following is the most potent anaphylatoxin?
A. C3a B. C4a C. C5a |
C.
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What events can initiate intracellular killing of pathogens? (2)
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1. IgG bind to Fcγ receptor
2. IFN-γ |
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What's the action of C3b or C4b binding with CR1?
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enhances intracellular killing, but not stimulate it.
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What cells have CR2(CD21)? (2)
What's the function of CR2 in these cells? |
B cell: strengthen B cell activation
FDC: long-term of B cell stimulation |
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Epstein-Barr virus(EBV):
1. what cells are infected? 2. how does the virus infect cells |
1. B cells
2. bind to CR2 |
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T/F: CR3 and CR4 are β-integrins that bind to iC3b.
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T.
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What the actions of CR3 or CR4 binding with iC3b? (2)
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1. Stimulate phagocytosis.
2. Adherence of leukocytes to endothelial cells in sites of inflammation. |
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The effect of CR1 and CR3 binding to C3b and iC3b respectively is similar: phagocytosis. What distinguishes these two?
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CR1 binding with C3b does not stimulate phagocytosis, initiation is required (ie. IFN-γ or IgG-FcγRI).
CR3 bind with iC3b doen't need additional help in stimulating phagocytosis. |
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CR1:antibody:antigen complex on erythrocyes are emliminated in what organs?
Mailfunction in the elimination would cause failure in ____. |
Liver and spleen: tissue macrophages.
Kidney: large complexes deposited on the podocyte. |
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What are the components of classical C5 convertase?
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C4b2a3b
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What are the components of alternative C5 convertase?
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C3b2Bb
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What is the funciton of C5?
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initiate formation of membrane attack complex.
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What feature of C5 is different from C3 and C4?
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no thioester bond.
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What complements are involved in forming membrane-attack complexes?
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C5: initate
C6: stabilized C5b, provide binding site for C7 C7: contain hydrophobic region that inserts into target cell membrane. C8: binds C5a,6,7, and inserts into target cell membrane. C9: polymerize to form a pore |
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A bacterium that produces an enzyme which degrades complement component C5a would most likely impair which of the following host defense?
A. ability of neutrophils to ingest bacteria. B. ability of cytotoxic T cells to kill infected host cells. C. initial activation of complement components. D. migration of neutrophils to the site of infection. E. release of complement proteins from the liver. |
D.
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What are anaphylatoxins? Give some examples.
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Compounds that cause acute systemic inflammatory response.
Examples: C5a, C3a, C4a |
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What specific actions do anaphylatoxin elicit? (2)
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1. induce smooth muscle contraction
2. degranulation of mast cells and basophils |
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What are some effects of C5a? (3)
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1. induce smooth muscle contraction
2. degranulation of mast cells and basophils 3. increase adherence of neutrophils and monocytes tp vessel wall, direct them to migrate to the site of antigen deposition. |
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The T cells that provide cytokine signals for B cell maturation:
A. CD4 Th0 cells B. CD4 Th1 cells C. CD4 Th2 cells D. CD8 precursor T cells E. CD8 CTLs |
C.
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What is passive immunity and how is it achieved?
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Transfer of preformed immunity from an immune subject to a nonimmune subject.
This can be achieved with transfer of whole serum, purified antibody, monoclonal antibody or intact effector or memory lymphocytes. |
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Define the antibody isotype involved in placental transfer and why is it important?
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IgG can provide passive protection in the blood stream and extracelular spaces of tissue until newborns make its own antibody.
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Define the antibody isotype in breast milk and why is it important?
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IgA pretects the newborn from colonization and invasion of ingested mirobes.
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Is it possible to transfer antureactive antibodies from a pregnant mother to her infant?
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Only if it's IgG. Treat: plasmaphresis.
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Which Ig is most important in protecting a baby of 2-months of age from common bacteria?
A. IgA B. IgD C. IgE D. IgG |
D.
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Why is IgG the most important Ig in protecting a baby of 2-months of age from common bacteria?
A. the lack of serum Ig proteases B. the long 1/2life of IgG molecule C. the long 1/2life of IgA D. the short 1/2life of IgM |
B
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What are the two categories of regulatory proteins in the plasma that limit the extent of complement activation?
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1. plasma proteins that control activation of complement
2. membrane proteins that regulate complement fixation |
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What are the three plasma proteins that regulates the activation of complement?
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1. C1 ihibitor(C1INH): binds C1r,s, inhibit clotting and kinin.
2. C4-binding protein(C4BP): bind to C4, making is susceptible to factor I. 3. Factor H: binds C3b, make it susceptible by factor I. |
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What is the cause of HANE(hereditary angioneurotic edema)?
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Defective C1INH.
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Name 2 vasoactive peptides.
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1. C2 kinin
2. bradykinine |
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T/F: C4BP that bind to C4b is competitive with C2a.
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T
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Name three membrane proteins that regulate complement fixation.
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1. DAF(decay-accelerating factor): bind to C4b, C3b, cause them to dissociate.
2. MCP(membrane cofactor prtein): bind to C4b, C3b, make them susceptible to factor I. 3. factor H 4. CR1 |
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What immune feature or component is most likely defective in a family that suffered bacterial meningitis caused by Neisseria meningitidis?
A. CD4 T cells B. complement protein factor I C. C8 D. IgG producing B cells E. NK cells |
C.
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