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85 Cards in this Set
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- Back
- 3rd side (hint)
where do naive lymphocytes arive from
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primary lymphoid tissue
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where are rearanged TCR (t cells) or IgG genes (B cells)
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naive lymphocytes
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what activates TH
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when they make contact with professional antigen presenting cells
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what are the most potent activator of TH
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conventional dendritic cells
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what activates CTL
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antigen specefic contact w/ dendritic cells and TH cells
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what are the pathways upon which B cells can be activated
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thymus dependent (antigen-specific contact w/ TH cells)
thymus independent(antigen specefic cross linking with surface IgM, no T cells involved) |
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what happens to T or B cells after they make contact w/ antigen
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they proliferate and differentiate into:
EFFECTORS - cells that do something Memory Cells - designed to presist, activated more readily by antigen |
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where are memory cells mainly found
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lymph nodes
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how long do effector cells live and why
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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
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where do naive lymphocytes encounter antigen
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2ndary lymphoid tissue, this is where they are activated, proliferate, and form a clone
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what also plays a role in TH cell activation other than Conventional dendritic cells
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macrophages
B cells |
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what is an example of a effector cell
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plasma cells (b/c they secrete antibodies)
TH cells (b/c they secrete cytokines) CTL (b/c they kill things) |
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what is the signal transduction pathway needed for lymphocyte activation
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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 |
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how can you measure the activation of PKC
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by measuring the amount present in the membrane/associated w/ the plasma membrane
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what activates PKC
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DAG and Ca
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what is the marker for all T cells
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CD3
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what is the marker for B cells
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CD19 and CD20
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what is the marker for NK cells
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CD56 or CD16
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what is the coreceptor for TH cells
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CD4
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what is the coreceptor for CTL
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CD8
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what is the range of WBC in body
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neutrophils
lymphocytes monocytes eosinophils basophils |
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what is the % of lymphocytes
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CD3 (T lymphocytes)
CD4 (TH) CD8 (CTL) CD19 or CD20 (B cells) CD3- or CD56 or CD16 (NK cells) |
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how do APC activate T cells
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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 |
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what is the purpose of adhesion molecules
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they stabalize cell to cell contact
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the does CD28 (T cell) bind to
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B7 (APC)
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what does CD40L ( T cell) bind to
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CD40 (APC)
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are adhesion molecules antigen specefic
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no they will act regardless of the peptide presented
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what is the importance of LFA3 and CD2
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a drug for the treatment of soriasis disrupts the interaction between LFA3 and CD2
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in T cells how is signal 1 sent
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TCR on T cell binds MHC peptide plus coreceptor (CD4 or CD8) on APC
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in T cells how is signal 2 sent
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B7.1/B7.2 (B7) on APC binds to CD28 on T cell
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what is the % of lymphocytes
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CD3 (T lymphocytes)
CD4 (TH) CD8 (CTL) CD19 or CD20 (B cells) CD3- or CD56 or CD16 (NK cells) |
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what signals are required for T cell activation
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signal 1 + signal 2
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how do APC activate T cells
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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 |
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what is the purpose of adhesion molecules
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they stabalize cell to cell contact
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the does CD28 (T cell) bind to
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B7 (APC)
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what does CD40L ( T cell) bind to
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CD40 (APC)
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are adhesion molecules antigen specefic
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no they will act regardless of the peptide presented
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what is the importance of LFA3 and CD2
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a drug for the treatment of soriasis disrupts the interaction between LFA3 and CD2
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in T cells how is signal 1 sent
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TCR on T cell binds MHC peptide plus coreceptor (CD4 or CD8) on APC
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in T cells how is signal 2 sent
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B7.1/B7.2 (B7) on APC binds to CD28 on T cell
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what signals are required for T cell activation
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signal 1 + signal 2
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what does CD40L do to APC
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it binds to CD40 on APC and causes the APC to make more B7 which serves as the amplification of activation of T cell
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what happens if someone lacks CD40L
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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
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what does LFA3 (APC) bind to
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CD2 (LFA2) - T cell
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what does ICAM1/2 (APC) bind to
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LFA1 (T cell)
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what does VCAM1 (APC) bind to
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VLA4 (T cell)
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how does co-stimulation occur
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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 |
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what do PRR and TLR induce during an infection
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B7
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what happens if an APC does not have B7
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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
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how does a APC lack of B7 reduce autoimmunity
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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 |
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what is an early even of TCR activation
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Tyrosine phosphorylation
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what occurs in Tyrosine phosphorylation
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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 |
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what does ZAP-70 activation lead to
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activation of Phospholypase C (PLC)
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what is the IL-2 critical for
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T cell activation
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what leads to making more IL-2
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NFkB and NFAT
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what happes in control of NFkB
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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 |
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what happens in control of NFAT
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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 |
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what are the downstream events that follow TCR signaling
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control of IL2 gene transcription
damping T cell enthusiasm |
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what is the dampening of T cell enthusiasm
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turning off T cells/immune system
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what occurs in the dampening oc T cell enthusiasm
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CTLA4 binds to B7 at the same site as CD28 on APC
-and since B7 only has one binding site CD28 competes with CTLA4 |
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what is CTLA4
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competitive antagonist
competes with CD28 to bind to B7 |
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what happens when CTLA4 binds to B7 and when CD28 binds to B7
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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 |
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what makes CTLA4 concentrations high
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CTLA4 concentrations are normally low but after activation of T cells the concentration on the surface increases
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what occurs when CTLA4 concentrations get high on the surface
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it competes with CD28 to bind to B7
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what does CTLA 4 basically do
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it blocks CD28 from binding to B7 meaning no signal (2) will be sent to activate the T cell
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家出
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/ running away from home/leaving home/(P)/
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[いえで]
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how are B cells activated
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by cross linking surface immunoglobins
Igalpha and IgBeta action required |
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what happens when antigen binds to b cell receptor
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increase PLC etc
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what is required for B cell activation
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Bruton's tyrosine kinase (BtK)
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what happens if you don't have BtK
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you can't make antibodies
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what are properties of Thymus independent antigen
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linear, repetitive structures (carbs/nucleic acid)
cross link surface IgM low affinity IgM secreted very poor memory similar to primary immune response |
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what do thymus independent antigen cells secrete
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only IgM therefore little class switching
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what are the properties of thymus dependent antigen
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requires thymus
requires action of TH cells |
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what are most protein antigens
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thymus dependent antigens
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what occurs in ANTIGEN PROCESSING BY B CELLS FOR THYMUS DEPENDENT ANTIGENS
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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) |
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what is signal 1 in Thymus dependent
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TCR and MHC2
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what is signal 2 in Thymus dependent
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CD40L of TH binds to CD40 of B cell
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what is signal 1 in Thymus independent
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surface IgM binds to Ag
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what is signal 2 in Thymus independent
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complement 3d (C3D)
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how is C3D involved in signal 2 of thymus independent
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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 |
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what does CR2 recognize
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C3d
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why can't B cells process thymus independent antigens
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because proteases don't act on repetitive strucutures (polysaccharides/nucleic acid/glycolipids) therefore no MHC presentation to T cells
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what can polysacharides do
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they can activate complement which leads to more C3D production and increases B cell activation
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natural antibodies against blood groups are
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thymus independent antigens
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what are examples of repetitive structures
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polysaccharides/glycolipids/nucleic acid
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