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93 Cards in this Set

  • Front
  • Back
what is the name of the process which is intiated by the fist time a naive T cell binds an antigen?
T cell activation
what is another name for T cell activation?
T cell priming
what are the three effector T cells?
1. Cytotoxic CD8 T cell
2. CD4 TH1 cell
3. CD4 TH2 cell
what are the preoffesional antigen presenting cells (APCs) responsible for bringing pathogen to the periphery to naive T cells
1. macrophages
2. dendritic cells
are macrophages or dendritic cells better at stimulating niave T cells?
dendritic cells
why are dendritic cells better activators of T cells?
they are mobile, thus can bind antigen then travel to a lymph node where as macrophages are resident cells
pathogens for which macrophages present antigens to T cells gain are located where?
macrophages are resident cells thus they must be located in the secondary lymphoid tissue to present antigen to T cells
dendritic cells in tissue are called?
immature dendritic cells
dendritic cells in lymph nodes are called?
mature or activated dendritic cells
where is the only place dendritic cells are found in the lymph node?
the cortex where the T cells are located
what is the site of entry for T cells in the lymph node?
the HEV's (high endothelial venules) -> the cortical region
what causes a T cell to stay in the lymph node?
binding of peptide/mHC complex that it recognizes
after binding of peptide/mHC complex that it recognizes, T cells do what?
proliferate and differentiate into clones of the themselves
after binding of peptide/mHC complex that it recognizes, how long does it take a T cell to begin proliferation?
a couple of days
how do effector T cells such as a TH2 or cytotoxic T cell leave the lymph node to go to the site of infection?
through the efferent lymphatic vessel
what are the 4 types of molecules that add in the passage of T cells into the lymph node from the HEVs?
1. selectics
2. vascular addressins
3. integrins
4. immunoglobulin superfamily proteins
what is the term that refers to the movement of niave T cells into the lymphoid tissue from HEVs?
homing
what are the 3 molecules necessary for homing to occur?
1. L-selectin (on T cell)
2. CD34 (a vascular addressin on endothelial cells)
3. GlyCAM-1 (a vascular addressin on endothelial cells)
binding of L-selectin to vascular adressin glycoproteins causes what to happen?
it slows the movement of the T lymphocyte through the HEV
what is the integrin that is on the surface of the T lymphocyte that aids in homing?
lymphocyte function associated antigen-1 (LFA-1)
what does LFA-1 bind to on the vascular cells of the HEVs to strengthen the initial selecting-vascular adressin binding?
two intracellular adhesion molecules called ICAM-1 and ICAM-2
what activates LFA-1 on the T lymphocyte?
CCL21
what is CCL21?
a soluble chemoattractant protein called a chemokine
what causes endothelial cells of the HEV to make CCL21?
binding of chemokine CCR7
what else produces CCL21 besides vascular endothelial cells?
stromal cell and dendritic cells
T cells LFA-1 binds to what on antigen presenting cells?
ICAM-1 and ICAM-2 on the antigen presenting cell surface
what does LFA-1 of on antigen-presenting cells bind?
ICAM-3 on the T cell surface
what strengthens the LFA-1/ICAM relationship between T cells and antigen-presenting cells?
the binding of CD2 on T cells with LFA-3 on antigen-presenting cells
when a cell finds an antigen/MHC complex it can bind to, what happens to the LFA-1 molecule?
their affinity for the ICAMs on the APC increases to become stable for several days
what distinguishes professional antigen-presenting cells from other antigen-presenting cells?
the presence of B7 co-stimulatory molecules on their surface
what are the 3 professional APCs?
1. dednritic cells
2. macrophages
3. B cells
where are denritic cells present in the lymph node?
only in the T cell area of the cortex
where are the B cells located?
only in the follicles
where are the macrophages located?
all throughout the medulla and cortex
which is more effective in presenting antigen to T cells, a B cell or a macrophage?
a macrophage
during times when there is no infection, what surface modification is made on professional APCs?
there is no surface B7 co-receptors
what is the surface receptor that dendritic cells use to take up antigen?
DEC 205
which of the professional APCs is the best at is most intergal in T cell response to a viral infection?
dendritic cells
what is the name of the immature dendritic cell located in the skin?
Langerhans' cells
what is the name of the large phagosomes contained in Langerhans' cells?
Birbecks granules
what is the name of the Langerhans' cells that enter the secondary lymphoid tissue?
mature dendritic cells or interdigitating reticular cells
what happens once a dendritic cell has taken up a mibrobial antigen?
it starts expressing By co-receptors and increases MHC molecules on the cell surface
which professional APC is responsible for taking up antigens that arrive at the lymph nodes in the lymph?
macrophages
what two functions does the macrophage serve by taking pathogens from the lymph?
keeps pathogens out of the blood and allows for pathegens to be presented to T cells
besides their role as a professional APC, what else do macrophages do in the lymph nodes?
consume and degrade the lymphocytes that die
while B7 co-receptors and MHC molecules are largely absent from macrophages when there is no infection, what innate immune machinery is still functioning?
receptors which recognize carbohydrates and other components of microbial surfaces
when an innate immunity receptor binds a ligand on the macrophage, what does the macrophage do?
it starts to express B7 co-receptors and increases expression of MHC molecules
where do most of the peptides presented by macrophages come from?
extracellular pathogens which will be presented on MHC class II molecules
what is the unique bacteria that actually uses the pathogen processing of macrophages to enter the cells and proliferate in the cytoplasm?
Listeria monocytogenes
what type of MHC molecule is most used by B cells?
MHC class II which means they mostly activate CD4 T cells
why are whole organisms along with the antigen of interest usually more effective vaccines?
becuase they have a co-stimulatory effect which is much stronger than purified antigen alone
what are the mibrobial components that are added to vaccines to cause co-stimulatory effects called?
adjuvants
when a TCR and MHC/peptide complex bind to each other what tells the T cell that peptide has been bound?
CD3 complex
what are the active parts of the CD3 complex proteins that stick out into the cytoplasmic side of the PM?
immunoreceptor tyrosine-based activation motifs (ITAMs)
what do ITAMs activate once peptide antigen is bound?
protein tyrosine kinases
what are the protein tails of the CD4 and CD8 co-receptors associated with on the cytoplasmic side of the PM?
protein tyrosine kinase called Lck
what does Lck activate when the CD4 or CD8 co-receptor is involved in binding of T cell with professional APC?
ZAP-70 which is a cytoplasmic protein tyrosine kinase
what does ZAP-70 bind to?
the phosphorylated zeta chain of the TCR
what is the minimum number of peptide/MHC complexes on a target cell to trigger a naive T cell?
100
in the absence of a co-receptor (CD4 or CD8) how many peptide/MHC complexes are needed to activate a niave T cell?
10,000 a 100 fold increase over normal
what are the 3 signaling pathways triggered by ZAP 70?
Production off transcriptional factos...
1. nuclear factor of activated T cells
2. NFcappaB
3. AP-1
what do the combined effects of nuclear factor of activated T cells, NFcappaB, and AP-1 cause to happen in T cells?
proliferation and development of effector function... the most important gene activation is for the production of cytokine IL-2
what does IL-2 do?
drives clonal expansion of T cells
in addition to binding the peptide/MHC complex, what other signal is needed for T cell activation?
the co-stimulatory signal
the co-stimulatory signal are delivered by which cells?
only professional APCs
what is the cell surface protein on niave T cells through which co-stimulatory signals are delivered?
CD28
what originates the co-stimulatory signal?
the B7 proteins on the professional APC surface
after the original binding of B7 by CD28, which new B7 is expressed on the niave T cell surface?
CTLA4
what is the function of CTLA4?
to dampen and limit cell proliferation
the production of IL2 is dependent on which 3 components?
1. TCR activation
2. co-receptor (CD4 or CD8)activation
3. co-stimulatory signal
how is over production of IL2 RNA protected against?
it is made to be very unstable
how does the co-stimulatory signal increase IL2 production? (2)
1. it stablizes the IL2 RNA transcipt so it is copied more times
2. it activates transcription factors which increase IL2 RNA production
by how much does the co-stimulatory signal increase IL2 production?
100 fold
how does cyclosporin A reduce the immune response to implanted organs?
it inhibits IL2 production by disrupting signals from the IL2 receptor
what happens to a T cell that binds self-peptide/MHC complex on a cell other than a professional APC?
it anergic becuase it receives no co-stimulatory signal because there are no B7 proteins present on cells other than professional APCs
the cytokines released by TH1 cells cause what 3 things to happen?
1. macrophage activation
2. inflammation
3. activate production of opsonizing antibodies
the cytokines released by TH2 cells cause what 2 things to happen?
1. B-cell differentiation
2. the production of neutralizing antibodies
a response biased toward TH1 cells is called?
cell-mediated immunity
a response biased toward TH2 cells is called?
humoral immunity
describe what controls the suppression of the TH1 and TH2 cells?
they each produce cytokines which suppress the other
patients with which T helper cell bias die fastest from leprosy, an intracellular pathogen?
TH2 bias becuase TH2 relies on specific antibodies, but these antibodies cannot access the pathogen inside the macrophage
which T cell type requires a stronger co-stimulatory effect, CD8 or CD4?
CD8
which are the only professional APCs capable of providing large enough co-stimulation to activate CD8 T cells?
dendritic cells
how does CD4 help stimulate CD8 when co-stimulatory signals are not strong enough from a professional APC?
when CD4 binds to a professional APC it releases cytokines which upregulate B7 proteins and increase the magnitude of the co-stimulatory signal
how do CD4 T cells help CD8 T cells proliferate even in the absence of a strong co-stimulatory signal?
CD4 T cells bind to a professional APC and release IL2. CD8 also bind, which causes the production of IL2 receptors, but not IL2. The CD8 IL2 receptors use the IL2 made by CD4 T cells to proliferate
how is the T cell effector function activate?
binding of the peptide/MHC complex on target cell
what is a major difference between mature and niave T cells in there requirements for activation?
mature T cells are activated independent of B7/CD28 interaction
why is i important for the requirement of co-stimulatory to be dropped for effector T cells?
it allows them to act on a larger variety of cells that present with their specific antigen peptide
how do mature T cells deal with the drop in surface ICAM1 and LFA3 on non-professional APC cells?
increase the expression of CD2 and LFA1 on their own surfaces
what is L-selectin replaced by in mature T cells?
VLA-4 which aids helps slow down T cells at the site of infection instead of HEVs
the molecules that carry out effector function fall into what two categories?
1. cytokines
2. cytotoxins
most of the cytokines made by T cells are called?
interleukins
tumor necrosis factor-alpha, CD40 ligand, and Fas ligand are considered to be what kind of cytokines?
membrane bound