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44 Cards in this Set

  • Front
  • Back
List the cells that are APCs
Monocytes
Macrophages
APC DCs (not follicular DCs)
B cell
List the cells that are phagocytes
Neutrophils
Monocytes
Macrophages
~Eosinophils
What is a 'left shift'
Neutrophilia. PMN>8,000
See lots of band cells (immature) indicates bacterial infection
Receptor/Marker Monocyte
CD14
LPS receptor
Receptor/Marker B cells
CD19, CD20, CD21
(EBV uses CD21)
Receptor/Marker T cells
Th
Tc
Treg
All=CD3,TCR
Th=CD4
Tc=CD8, CTL
Treg=CD4, CD25
Receptor/Marker NK cells
CD16a
CD57
Receptor/Marker Mast cells
IgE receptor
C3a receptor
Receptor/Marker Basophils
IgE receptor
C3a receptor
Amount of Cells in WBC
Neutrophils
Love (lymphocytes)
Making (macrophages)
Everything (eosinophils)
Better (basophils)
Th function
produce cytokines
Treg function
limit immune response and control auto-reactive lymphocytes
Tc function
direct cell killing of tumor cells and virally infected cells
(MHC restricted)
Lymph node
lymphocyte path
antigen paht
Lymphocytes enter via arterial blood and leave via efferent lymphatic vessel
Ag (often with DC) enter node via HEV (T/B cells bind L-selectin to enter HEV)
Spleen
lymphocyte path
Ag path
Lymphocytes enter via marginal sinus- B cells->follicles T cells -> PALS
Ag enter via splenic a and trapped by splenic DC/macrophages
Defensin structure
amphipathic
aa chains + hydrophobic aa chains
Allows interaction with meicrobial membranes --> microbial pores
Defensins in SI and epithelial surfaces
Cytokines inducing myeloid stem line + what cells come from this line?
IL3 + GM-CSF

erthrocytes, megakaryocytes (platelets), basophils, eosinophils, neutrophils, granulocyte-monocyte progenitor --> neutrophil + monocyte
(monocyte-->macrophage + DC)
Cytokines inducing Lymphoid stem line + what cells come from this line?
IL3 + IL7
T cells, B cells, NK cells
Synthesis of NO
L-arginine + O2 --> L-citrulline + NO
Done by NOS
Syntesis of superoxide anion, H2O2, ClO-
NADPH + 2O2 --> NADP+ + 2O2- + H+
Done by NADPH oxidase
Pathogen binds TLR --> stimulates what TFs
And function of TF?
Where are TLRs found?
NK-kB + IRF-3
NK-kB involved in costimulation
IRF-3 stimulates type 1 interferons
TLRs on mostly innate cells
What is costimulation?
NK-kB causes APCs to upregulate cell surface expression of costimulatory molecules B7 molecules: CD80 and CD86
This is necessary (along with MHCs) to activate T cells
Type 1 interferons:
Released by? In response to?
3 functions?
IFNa + INF-B
Released by macrophages in response to viral components binding TLRs.

[can use interferons to treat viral infections (viral hepatitis)]
1. Induce resistance to viral replication in all cells
2. Increase expression of ligands for NK cell receptors
3. Activate NK cells to kill virus-infected cells
NK Cell's granules
Perforin - monomers polymerize to form channel
Granzymes - serine esterases, granzymes enter target cell through perforin channel and activate caspases (involved in apoptotic pathway)
Functions of cytokines:
Pleiotropism?
Redundency?
Synergy?
Antagonism?
P: one cytokine has multiple effects
R: many cytokines do the same function
S: cytokines work together to function
A: cytokines can have opposite effects
IFN-y
Released by?
Acts on? - function?
Th2 Cells?
Macrophage?
DC
NK
B cell
CD4 Th1 Cells, Tc Cells, + NK cells
MAJOR FUNCTION = INCREASED MICROBICIDAL ACTIVITY OF MACROPHAGES
Th2 = decreased proliferation and production of IL-4 + IL-5
Macrophage = INCREASED MICROBICIDAL ACTIVITY, increased expression of MHC II
DC= increased exp of MHC II
NK= increased cytotoxic activity
B cell= increased differentiation and Ab production
C' Classical Pathway starts with
Activated by immune complexes binding C1 complex
Requires Ab:Ag complexes on pathogen surfaces
C3 convertasse = C4b2b
C' MB-lectin Pathway
Requires mannose binding lectin to bind pathogen. Macrophages timulate liver to secrete acute phase proteins including mannose-binding lectin (MBL)
C3 convertase = C4b2b
C' Alternative Pathway
Pathogen induced spontaneous cleave of C3.
C3 convertase = C3bBb
Deficiency in C1 inhibitor
What is it?
Sx?
Hereditary Angiodedema
C1 remains active - continuous creation of C3 and C5 convertasses. Get lots of C3a/C5a anaphylatoxins
Sx: excessive swelling at sites of bacterial entry (airways - get asphyxiation/death)
Defect in cell surface expression DAF and CD59
normalling keeps MACs from forming
Get excess C' activation - especially on RBC surfaces
Get recurrent bouts of intravascular hemolysis --> hemolytic anemai + venous thrombosis
5 signs of inflammation
heat, redness, edema, pain, loss of function
Extravasation Process
1. Rolling Adhesion =
Leukocyte has selectin ligand that binds selectin on endothelium (endothelial expression of E and P-selectins is rapidly upregulated by TNF and IL-1)
2. Integrin activation =
Integrins on leukocyte are activated by chemokines
3. Stable adhesion =
High affinity integrins on leuokocyte have strong interaction with CAM on endothelium.
LAD-1
LAD-2
(leukocyte adhesion deficiencies)
LAD-1: failure of WBC expression of CD18 = B2 chain of integrins
LAD-2: failure in expression of CD15s sialyl Lewis-X = ligand for E and P selectins
Sx: pts have elevated WBCs with recurrent apustualr bacterial infections (delayed umbilical cord seperation)
IL-12
Secreted by:
Local Action:
S: tissue macrophages in response to Ag
LA: NK cell activation; induces differentiation of CD4 T cells into Th1 cells
IL-8
Secreted by:
Local Action
Tissue macrophages is response to Ag
LA: chemoattractant for WBCs= neutrophils, basophils and T cells to site of infection
IL-1
Local Action:
Systemic Action:
LA: Activates vascular endothelium (upregulates E and P selectins), activates lymphocytes, local tissue, destruction increases access of effector cells
SA: Fever production of IL-6
TNF-a
Local Action:
Systemic Action:
LA: Activates vascular endothelium and permeability (upregulates E and P-selectin on endotheium), leads to increased entry of IgG, C' and cells to tissue and increased fluid drainage to lymph nodes
SA: fever mobilization of metabolites, Shock
IL-6
Local Action:
Systemic Action:
LA: Lymphocyte activation, increased Ab production
SA: fever induces acute-phase protein production
IFN-y
Local Action:
Secreted by:
LA: Drives granulomatous infalmmation
S: Th cells
Granulomatous Inflammation is driven by what cells producing which cytokine?
Th cells producing IFN-y - which stimulates macrophages to become epithelioid cells.
2 examples of a mitogen
LPS
Superantigen
3 examples of a hapten
Poison Ivy
Penicillin
Conjugate vaccines
4 things that affect variability of immune response among different people
physical state of Ag
biological/therapeutic manipulation of the immune response
Genetics
'holes' in the immune system