Lecture 14 Flashcards
(18 cards)
What immunoglobin classes predominate in blood?
IgG and IgM
What immunoglobin class predominates in secretions across epithelia?
Dimeric IgA
How does a fetus receive IgG from the mother?
transplacental transport
Where is IgE found? What cell type does it associate with?
associated with mast cells just beneath epithelial surfaces
Where is IgA synthesized and where is it transported?
synthesized by plasma cells in the lamina propria, transported into lumen of gut through epithelial cells at base of crypts
What is used to transport IgA across epithelial cells?
plgR
How does IgA act as an antigen-specific barrier in the gut lumen?
dimerizes, binds to layer of mucus overlaying gut epithelium
How does neutralization of toxins occur?
IgG antibodies block binding of toxin to cellular receptors (no endocytosis/dissociation of toxin)
How do antibodies neutralize viral infection?
bind to viral surface proteins, inhibiting initial binding to the cell or its subsequent entry
How do antibodies neutralize bacterial infection?
(on mucosal surfaces) bacteria bind to cell surface via adhesins, antibodies against adhesins block colonization and uptake
What is the purpose of the “staple conformation” of IgM?
several identical epitopes bound by IgM on a pathogen surface bends conformation, allowing globular heads of C1q to bind to Fc regions of IgM
What can happen when multiple IgG molecules bind to antigens on the bacterial surface?
single molecule of C1q to two or more Fc regions
What happens after C1q binds to the Fc region>?
conformational change activates associated C1r –> cleaves pro-enzyme C1s –> generates serine protease that initiates complement cascade
How do antibody-coated bacteria become degraded?
IgG bind, allowing phagocyte recognition through Fc receptors, complement proteins coat and bind complement receptors
How do free antibodies avoid activation?
do not strongly bind Fc receptors (FcRs) so do not crosslink
How does cross-linking FcRs trigger responses?
Antigen-bound antibodies bind a target in a cluster on the surface –> simultaneously bind multiple FcRs
Activating FcRs (ITAM motifs) send signals for phagocytosis, degranulation, cytokine release
Inhibitory FcRs (ITIM motifs) suppress immune activation, preventing excessive inflammation
How do NK cells kill?
large granular non-T, non-B lymphoid cells with FcγRIII (CD16) on surface, when encounter cells coated in IgG, rapidly kill target cell
How do IgE and mast cells interact?
cross-linking of IgE through binding to high affinity receptor FcεRI –> rapid degranulation –> inflammatory mediator release
