Chapter 9 Flashcards
do antibodies in different locations function the same or differently
differently
antibodies in the blood, lymph, and extracellular fluids function how
by binding microbes -> aggregation, neutralization, and complement activation
antibodies in mucusal surface function how
by trapping microbes in the mucus layer
b cell activation generating high affinity receptors would include what
somatic hypermutation and affinity maturation
what cells do somatic hypermutation
TFH cells
what cells do affinity maturation
FDCs
b cell activation becoming antibody factories (plasma cells) include
class switching
what cells are involved in class switching
TFH cells
where does cross-linking BCR inducing signaling occur
secondary lympoid organs
BCR binds multiple what on the surface of microbes
epitopes
what does the binding of epitopes result in
cross-linking BCRs
after the BCR binds multiple epitopes on the surface of microbes creating cross linking what happens
kinase of ITAMS on Ig alpha/beta
after the BCR binds multiple epitopes on the surface of microbes creating cross linking what happens and kinase of ITAMs on Ig alpha/ beta what happens
activation signals are sent to the nucleus and create in gene expression
what does CR2 do
bind to Ag via C3d
what is CD19
signaling domain
what is CD81
membrane localization of complex
CR1 (b cell) binds what and on what
C3b on pathogen
once CR1 binds Csb on pathogen what is recruited
factor I
what does factor I do
cleaves C3b-> iCsb -> C3d
what does C3d bind
CR2
B cell signaling for whole microbe
- BCR bind to antigen
- coreceptor bind C3d
- signaling from BCR and coreceptor converge
b cell signaling for part of microbe
- BCR bind a component of microbe
- C3d binds to same component and CR2
- converge on signaling
2 ways to activate B cellls is
thymus independent and dependent
thymus independent includes what b cells
B1 and B2
thymus dependent includes what b cells
only b2 cells
thymus (t cell) independent has no
TFH cell help: only make low affinity IgM Ab
thymus (t cell) depenedent has
TFH cell help:
high affinity receptors (somatic hypermutation and affinity maturation)
class switch
steps for B cell activatioin by a thymus independent antigen
- BCR cross-linking
- co-receptor and BCR signaling
- become IgM plasma cell-> low affinity
what stores antigens
FDCs
FDC- not derived from
hematopoiesis
where are FDCs derived from
stromal cells and bone marrow
what do fdcs so
capture antigen and store on surface
dendrites have what receptors
complement: CR1 and CR2
is CR1 or CR2 dominant
CR2
FDCs lack
phagocytic activity
antigens are captured by
macrophages or FDC
three steps to how antigens are captured by macrophages or FDC
- free Ag enter via afferent lymph vessels
- in subcapsular sinus they can be trapped by macrophage or
- move into B cell zone and be trapped by FDCs
primary focus b cells secrete IgM where
medullary chords
proliferation of primary focus B cells (2) options
plasmablast that secrete IgM
or
plasmablast tha continue differentiation and move to primary follicle
what antibody effectors bind IgG
FcRn
Fc gamma RI
Fc gamma RIIA
Fc gamma RIIIB
Fc gamma RIII
what antibody effector binds IgE
Fc epsilon RI
what antibody effector binds IgA
Fc alpha RI
what does transcytosis across endothelial cells mean
moving IgG from blood
ITAMS are
activating
ITIMs are
inhibitory
4 steps for transcytosis across endothelial cells
- IgG binds FcRn on luminal side of endothelial cell
- IgG and FcRn endocytosed
- the vesicle is transported to tissue side of the cell
- release content outside of the cell
polygR binds and what does it interact with
J chain and interacts IgA and IgM
transcytosis through epithelial cells means
crossing epithelial cell tissues->mucus
steps for how poly-Ig uses transcytosis through epithelial cells
- polygR bind to J chain
- endocytosis
- vesicle transported from bottom to top of cell
- vesicle fuses with plasma membrane of apical side to release Ab into mucus
IgE protects from
parasites
what WBC help fight parasites
eosinophil
basophil
mast cell
during primary infection what is made
IgE
IgE binds what on eosinophils
FcERI
what happens in secondary infection
preloaded eosinophils will bind the parasite using IgE-> degranulation
when IgG binds during IgE parasite infection what does it do
decrease inflammation
Fc gamma RII B2->
mast cells
Fc gamma RII B1->
macrophages, neutrophils, eosinophils
maternal antibodies are transferred to
fetus/ newborn
what crosses the placenta
IgG
how does IgG cross the placenta
FcRn
what is secreted into breastmilk
IgA
once IgA is secreted into breastmilk it is transferred to
new born
steps for neutralization of virus immune
- virus enters
- IgA will bind virus
- virus can’t interact with receptor-> doesnt enter cell-> no infection
steps for neutralization of non-immune cell
- virus enters
- attachment protein binds to receptor
- virus enters-> infection
what binds bacteria in immune cells
IgA
what interacts with non-immune cells
bacteria
what happens when IgA binds bactera in immune cells
bacteria cant bind cells to infect issues
what happens when bacteria binds non-immune cells
replication and cause infections
when a toxin binds receptor what happens
endocytosis of toxin
when the toxin is endocytosed what happens
active part of toxin is released into cytoplasm and there is a bad outcome
is there is neutralization of the toxin what happens
Ab binds toxin and prevents the toxin from binding cells which results in no diseases
IgM binding to antigen on a pathogen surface initiates the
classical pathway of complement activation
planar form of IgM is
flat
staple form of IgM is
bent at hinge region
C1 binds to only what form of IgM
staple
the binding of C1 to staple IgM initiates
classical pathway
outcomes of classical pathway
phagocytosis
inflammation
pores
phagocytosis expresses
C3b
inflammation expresses
C3a
pores express
C5b
multiple IgGs are bound to
microbe and C1
steps for clearing immune complexes
- Ab bind Ag (not whole microbes)
- C1q bind to start complement
- C3b deposited on Ag and Ab
- Ab/ Ag-C3b complex binds CR1 on RBCs
- complexes filter out in spleen and liver
- macrophagaes will phagocytose complex
Ab-mediated opsonization
- Ab binds to microbe
- Ab binds Fc receptor
- signaling
- phagocytosis
- microbe destroyed
what Fcy receptors are for inhibitation
FcyRIIB2 and B1
Ab dependent cell-mediated cytotoxicity steps
- tumor cell binds Ab
- Ab binds FcyRIII on Nk cells
- NK cells release granules (perfornin and granzyme)
- tumor cell dies by apoptosis