Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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
|