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85 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
where do naive lymphocytes arive from
primary lymphoid tissue
where are rearanged TCR (t cells) or IgG genes (B cells)
naive lymphocytes
what activates TH
when they make contact with professional antigen presenting cells
what are the most potent activator of TH
conventional dendritic cells
what activates CTL
antigen specefic contact w/ dendritic cells and TH cells
what are the pathways upon which B cells can be activated
thymus dependent (antigen-specific contact w/ TH cells)
thymus independent(antigen specefic cross linking with surface IgM, no T cells involved)
what happens to T or B cells after they make contact w/ antigen
they proliferate and differentiate into:

EFFECTORS - cells that do something

Memory Cells - designed to presist, activated more readily by antigen
where are memory cells mainly found
lymph nodes
how long do effector cells live and why
they are short lived because after immune response to inflammation/infection and it has gone away the immune response must be turned down, not good to have it persist
where do naive lymphocytes encounter antigen
2ndary lymphoid tissue, this is where they are activated, proliferate, and form a clone
what also plays a role in TH cell activation other than Conventional dendritic cells
macrophages
B cells
what is an example of a effector cell
plasma cells (b/c they secrete antibodies)
TH cells (b/c they secrete cytokines)
CTL (b/c they kill things)
what is the signal transduction pathway needed for lymphocyte activation
phospholipase C (PLC)
-becomes active after antigen specefic receptors bind and digests lipids in the membrane (PIP2)

PIP2
-breaks down into DAG which stays in the membrane
OR
-breaks down into IP3 which enters the cytoplasm

IP3
-binds to Ca releasing channel and caueses the release of stored Ca in ER into the cytoplasm

Ca binds to Protein Kinase C

Protein Kinase C also binds to DAG and becomes attached to the membrane

once PKC is in the membrane it can start to phosphorylate proteins/substrates
how can you measure the activation of PKC
by measuring the amount present in the membrane/associated w/ the plasma membrane
what activates PKC
DAG and Ca
what is the marker for all T cells
CD3
what is the marker for B cells
CD19 and CD20
what is the marker for NK cells
CD56 or CD16
what is the coreceptor for TH cells
CD4
what is the coreceptor for CTL
CD8
what is the range of WBC in body
neutrophils
lymphocytes
monocytes
eosinophils
basophils
what is the % of lymphocytes
CD3 (T lymphocytes)

CD4 (TH)
CD8 (CTL)
CD19 or CD20 (B cells)
CD3- or CD56 or CD16 (NK cells)
how do APC activate T cells
via direct cell to cell contact involving pairs of proteins

1) TCR recognizes MHC peptides on APC (recognition event in which signal is sent to interior of T cell)

2) adhesion molecules are there to stabalize cell to cell contact
what is the purpose of adhesion molecules
they stabalize cell to cell contact
the does CD28 (T cell) bind to
B7 (APC)
what does CD40L ( T cell) bind to
CD40 (APC)
are adhesion molecules antigen specefic
no they will act regardless of the peptide presented
what is the importance of LFA3 and CD2
a drug for the treatment of soriasis disrupts the interaction between LFA3 and CD2
in T cells how is signal 1 sent
TCR on T cell binds MHC peptide plus coreceptor (CD4 or CD8) on APC
in T cells how is signal 2 sent
B7.1/B7.2 (B7) on APC binds to CD28 on T cell
what is the % of lymphocytes
CD3 (T lymphocytes)

CD4 (TH)
CD8 (CTL)
CD19 or CD20 (B cells)
CD3- or CD56 or CD16 (NK cells)
what signals are required for T cell activation
signal 1 + signal 2
how do APC activate T cells
via direct cell to cell contact involving pairs of proteins

1) TCR recognizes MHC peptides on APC (recognition event in which signal is sent to interior of T cell)

2) adhesion molecules are there to stabalize cell to cell contact
what is the purpose of adhesion molecules
they stabalize cell to cell contact
the does CD28 (T cell) bind to
B7 (APC)
what does CD40L ( T cell) bind to
CD40 (APC)
are adhesion molecules antigen specefic
no they will act regardless of the peptide presented
what is the importance of LFA3 and CD2
a drug for the treatment of soriasis disrupts the interaction between LFA3 and CD2
in T cells how is signal 1 sent
TCR on T cell binds MHC peptide plus coreceptor (CD4 or CD8) on APC
in T cells how is signal 2 sent
B7.1/B7.2 (B7) on APC binds to CD28 on T cell
what signals are required for T cell activation
signal 1 + signal 2
what does CD40L do to APC
it binds to CD40 on APC and causes the APC to make more B7 which serves as the amplification of activation of T cell
what happens if someone lacks CD40L
they then can't make immunoglobins because CD40L is needed in order to T helper cells to bind to B cells and help them make antibodies
what does LFA3 (APC) bind to
CD2 (LFA2) - T cell
what does ICAM1/2 (APC) bind to
LFA1 (T cell)
what does VCAM1 (APC) bind to
VLA4 (T cell)
how does co-stimulation occur
APC can respond to danger signals from infections because they have PRR and TLR

when APC comes into contact w/ T cell they have MHC 1 (signal 1) and B7 (signal 2) which activate the T lymphocyes
what do PRR and TLR induce during an infection
B7
what happens if an APC does not have B7
if a APC presents a antigen to T cell the T cell won't become activated because there is no sending of signal 2 and the T cell will be ANERGIC
how does a APC lack of B7 reduce autoimmunity
dendritic cells endocytize a lot of proteins and as a result may take up our own proteins and present them to T cells, but since those proteins don't cause an infection/inflammation no danger signal will be sent and no B7 to activate the T cell

these T cells are anergic
what is an early even of TCR activation
Tyrosine phosphorylation
what occurs in Tyrosine phosphorylation
TCR-CD3/4/8 complex activates LCK

LCK phosphorylates Zeta chain of CD3

Zeta chain of CD3 BINDS to ZAP-70

binding of Zeta chain of CD3 to ZAP-70 leads to Protein Kinase activity to continue signal cascade downstream
what does ZAP-70 activation lead to
activation of Phospholypase C (PLC)
what is the IL-2 critical for
T cell activation
what leads to making more IL-2
NFkB and NFAT
what happes in control of NFkB
increase activation of PLC

increase Ca and DAG

PKC activation

PKC phosphorylates IkB

phosphorylation of IkB causes the release of NFkB into the cytoplasm

NFkB goes to the nucleus and causes increase in IL-2 gene transcription
what happens in control of NFAT
PLC activation

increase Ca

INCREASE CALCINEURIN

Calcineurin is a phosphatase and will remove phosphate group from NFAT

after NFAT loses the phosphate group it can enter the nucleus

NFAT in the nucleus causes increase in IL2 transcription/activation
what are the downstream events that follow TCR signaling
control of IL2 gene transcription

damping T cell enthusiasm
what is the dampening of T cell enthusiasm
turning off T cells/immune system
what occurs in the dampening oc T cell enthusiasm
CTLA4 binds to B7 at the same site as CD28 on APC
-and since B7 only has one binding site CD28 competes with CTLA4
what is CTLA4
competitive antagonist

competes with CD28 to bind to B7
what happens when CTLA4 binds to B7 and when CD28 binds to B7
when CTLA4 binds nothing happens b/c CTLA4 can't send signals to the T cell (ONLY CD28 CAN)

when CD28 binds it sends a signal that enhances the activation of T cells
what makes CTLA4 concentrations high
CTLA4 concentrations are normally low but after activation of T cells the concentration on the surface increases
what occurs when CTLA4 concentrations get high on the surface
it competes with CD28 to bind to B7
what does CTLA 4 basically do
it blocks CD28 from binding to B7 meaning no signal (2) will be sent to activate the T cell
家出
/ running away from home/leaving home/(P)/
[いえで]
how are B cells activated
by cross linking surface immunoglobins

Igalpha and IgBeta action required
what happens when antigen binds to b cell receptor
increase PLC etc
what is required for B cell activation
Bruton's tyrosine kinase (BtK)
what happens if you don't have BtK
you can't make antibodies
what are properties of Thymus independent antigen
linear, repetitive structures (carbs/nucleic acid)
cross link surface IgM
low affinity IgM secreted
very poor memory
similar to primary immune response
what do thymus independent antigen cells secrete
only IgM therefore little class switching
what are the properties of thymus dependent antigen
requires thymus
requires action of TH cells
what are most protein antigens
thymus dependent antigens
what occurs in ANTIGEN PROCESSING BY B CELLS FOR THYMUS DEPENDENT ANTIGENS
Ag binds to surface IgM

Ag-IgM complex signals and is then endocytosed

Antigen degraded and peptides bind the MHC2

antigens presented to cell (TH)
what is signal 1 in Thymus dependent
TCR and MHC2
what is signal 2 in Thymus dependent
CD40L of TH binds to CD40 of B cell
what is signal 1 in Thymus independent
surface IgM binds to Ag
what is signal 2 in Thymus independent
complement 3d (C3D)
how is C3D involved in signal 2 of thymus independent
C3d bind to the pathogen and has determinante that bind to IgM

pathogen binds to IgM and CR2

IgM comes together w/ CR2 to form signaling complex

generated signals mediate B cell activation
what does CR2 recognize
C3d
why can't B cells process thymus independent antigens
because proteases don't act on repetitive strucutures (polysaccharides/nucleic acid/glycolipids) therefore no MHC presentation to T cells
what can polysacharides do
they can activate complement which leads to more C3D production and increases B cell activation
natural antibodies against blood groups are
thymus independent antigens
what are examples of repetitive structures
polysaccharides/glycolipids/nucleic acid