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107 Cards in this Set

  • Front
  • Back
B cells
derived from common lymphoid progenitor
-make antibodies
-a protein that can bind to an antigen and illicit an immune response
T cells
derived from common lymphoid progenitor
-CD4+ = helper T cells or regulatory T cells
-CD8+ = cytotoxic T lymphocyte
CD4+
helper T cells
-tell other cells what to do by secreting certain things

regulatory T cells
-supress an immune response
CD8+
cytotoxic T lymphocyte (killer T cells)
-go out and actually kill infected cells
-cell surface proteins expressed on T cells
-cluster of differentiation
lymphocyte
B and T cells
NK cells
natural killer cells
-find infected cells and kill them
-first ones, in innate immunity
eosionophil
derived from common granulocyte precursor
- granules contain basic molecules
-only when responding to parasites allergies
basophil
derived from common granulocyte precursor
-basic granules
-parasitic/allergic response activate certain b cell response
neutrophils
derived from common granulocyte precursor
-phagoytosis
- made all the time
-can do one round of phagocytosis and then die
-need lots of them
-develop in bone marrow, enter blood stream
macrophages
derived from monocytes
-macrophage once in circulation
-capable of many rounds of phagocytosis
-Antigen presenting cells
-recognizes pathogen, triggers txn of cytokines - imflammatory response
dendritic cells
derived from myeloid progenitor
-have dendrites
-Ag presenting cells that activate T cells
-can do phagocytosis but only so they can do Ag presenting to T cells
mast cells
derived from myeloid progenitor
-have granules
-parasitic/allergic response
-contain histamine
what cells have APC function
macrophages, B cells, and dendritic cells
what cells have phagocytic function
macrophages, neutrophils
what cells have killing function
natural killer cells and cytotoxic t lymphocytes
what cells are involved in allergic and parasitic response
eosinophil, basophil and mast cells
What is the cell type that gives rise to all different cell types in the blood?
pluripotent hematopoietic stem cell
function of the hematopoietic stem cell
has potiential to become any of the cells of the blood
after the hematopoietic stem cell - what are the three possibilities?
common _______ progenitor

-lymphoid
-myeloid
-erythroid megakaryocyte
what comes out of the common lymphoid progenitor line
NK/T cell precursor - becomes T cells and NK cells

and B cells - become plasma cells
what comes out of the common myeloid progenitor line
common granulocyte precorsor and "unknown precursor"
what comes out of the common granulocyte precursor line
neutrophil
basophil
eosinophil
what comes out of the "unknown precursor line of the common myeloid progenitor line?
monocytes - become dendritic cells and macrophages

and mast cells
what comes out of the common erythroid megakaryocyte progenitor line
megakaryocytes and erythroblasts
function of the megakaryocyte
platelet formation and wound repair
function of the erythrocyte
oxygen transport
what are the functions of b cells
production of antibodies
plasma cell = fully differentiated B cell that secretes antibodies
what are the types of t cells
cytotoxic t lymphocyte (CD8+)

helper T or T regs (CD4+)
what are the functions of NK cells
kills cells infected with certain viruses

involved in innate immunity

see if theres a problem and CTL comes in later
function of eosinophil
killing of Ab-coated parasites through release of granule contents
function of basophil
controlling immune responses to parasites
function of neutrophil
phagocytosis and killing of microorgansims
what is the function of T regs
what is the function of helper t cells

what are their numbers
supress an immune response

tell other cells what to do by secreting certain things

CD4 = helper T and T regs
CD8 = CTLs
what is a monocyte
circulating precursor cell to macrophage
function of macrophage
phagocytosis and killing of microorganisms

activation of t cells an initiation of immune response
stages of T cell development in the thymus
DN1 - TCR genes in germline configuration
DN2 - Beta chain rearrangements (DJ recombination)
DN3 - Beta chain rearrangements (V-DJ recombination starts expressing pre-t cell receptor
DN4 - proliferation pre-t cell receptor stimulation

Double positive stage - CD4 and CD8 expressed on surface ( with pre-t receptor. alpha chain rearrangements (just D and J). TCR expressed on cell surface with CD4 and CD8. positive and negative selection.

Single positive stage - turning off of either CD4 or CD8 (lineage commitment)
discuss the mechanisms by which a BCR Ag binding specificity is generated. use bullet points
1. VJ light chain rearrangement + VDJ heavy chain rearrangement - multiple copies of V, D, and J regions found on different loci
2. pairing of different H and L chains
3. Junctional Diversity - strands are cut, bent into hairpin, ends are cleaved, TdT adds NTs to extend ends of cleaved hairpins, strands are paired, gaps are filled. really changes the BCR and creates infinite possibilities
4. somatic hypermutation - improve Ab binding on gene level by AID.. after Ag encounter
5. isotype switching - IgM is default (at maturation). switch to IgG, IgA, or IgE ( after Ag encounter). switch sequences between C regions. when switch sequences join they cut out middle parts
sequences of events from t-cell in thymus to TH1 cell activating macrophages
Thymus
naiive - has only gamma and beta chains - bind IL2 with moderate affinity
activated - has gamma, beta, and alpha chains - bind IL2 with high affinity
proliferation
immature effector CD4 t cell
interacts with macrophage
-MCH-II binds CD4/TCR
-CD40 binds CD40 Ligand
-IFN-gamma receptor binds IFN-gamma

activation of Tcell and kills macrophage
sequences of events from tcell in thymus and b cell in bone marrow to TH2 cell and b cell activation
Thymus
naiive - has only gamma and beta chains - bind IL2 with moderate affinity
activated - has gamma, beta, and alpha chains - bind IL2 with high affinity
proliferation
immature effector CD4 t cell

B cell leaves bone marrow
b cell encounters Ag from FDC presentation
enters LN
presents Ag on its MHC-II
B cell binds TH2 cell

LFA-1 binds ICAM-1 on B cell
CD4/TCR binds MHCII
CD40L binds CD40 on B cell

helper T reorients cellular machinery secreting cytokines towards B cell

b and t cells proliferate

b cells differentiate in to plasma cells and start secreting Abs
what are the different antibody isotypes, what is their function, and what is their distribution in the body?
IgM - complement, pentamer, found in heart or circulation

IgG - neutralization, complement, phagocytosis/opsonization - found everywhere, blood, in utero

IgA - neutralization, dimer= mucosal area and in baby from mother, monomer = everywhere,

IgE - allergic response, found in connective tissues
How do pathogens evade the immune system? list and discuss all of the examples
genetic variation with in species (sterotypes)

mutation and recombination (antigenic drift and antigenic shift)

rearrangement and changes in Ag (trypanosome- a parasite infecting only humans)

viral latency (not active until triggered, herpes, chicken pox)

subversion/sabotage of hose immune system (inhibit normal immune machinery, use human proteins)
list all of the inherited immunodeficiency diseases?
antibody defects (XLA, selective IgA deficiency, or hyper-IgM syndrome)

compliment pathway defects (immune complex issues, DAF and CD59 defects, CI-inhibitor defects)

Phagocytic cell defects (LAD, Chronic granulomatous disease, chediak-higashi syndrome)

T-cell defects (gammaC defect, ADA, bare lymphocyte syndrome, digeorge syndrome)
XLA
an Ab defect

Btk deficient (necessary for b cell development) therefore no Abs
selective IgA deficiency
an Ab defect

have every ag isotype except igA therefore more mucosal infections
hyper IgM syndrome
an Ab defect

make IgM but cant do isotype switching due to a mutation in CD40L on t cell. therefore cant activate B cells
immune complex issues
compliment pathway defect

have trouble clearing the immune complexes by RBCs (Ag-Ab complex)
DAF and CD59 defects
compliment pathway defect

compliment inhibitiors that make sure you dont kill own cells are defective. therefore you set compliment on own cells, esp RBCs
Ci-inhibitor defects
compliment pathway defect

uncontrolled C2 cleavage and C2b overproduction. can get uncontrolled C2 cleavage too much causes inflamation and vaso-dialation, fluid leaks, fluid accumulation in lungs
LAD
phagocytic cell defects

mutation in integrin (bind to glycams so the cell can get intot he SLT) so that now lymphocytes can circulate but can never get into the site of infection
chronic granulomatous disease
phagocytic cell defects

oxygen radial production is inhibited
problem making granulomatas causing apoptosis in infected cell
chediak higashi syndrome
phagocytic cell defects

problem forming vesicles or fusing vesicles
gamma c defect
t cell defect

defect in gamma chain of IL2 receptor

IL2 cant bind with high affinity and therefore cells cant proliferate
ADA
t cell defect

enzyme deficiency where metabolism pathway doesnt work properly so you get a build up of one of the by products which are toxic to T cells
bare lymphocyte syndrome
t cell defect

do not have any mhc-II expressed on the surface therefore you cant present Ags
digeorge syndrome
thymic epithelium that develops improperly therefore have improper tcell development
modes of HIV transmission
contaminated blood product
intercourse
dirty needles
maternal fetal transfer - birth or breast milk
course of HIV and development of aids
infection
flu-like symptoms (sometimes) for 2-6 weeks
then an asymptomatic phase
then a symptomatic phase
then AIDS

CD4 T cell count is slowly going down
mechanism of CD4 t cell depletion in HIV infection
direct viral lysis: virus infects cell, makes copies, start infecting other cells, causing direct lysis. cd4 cells more susceptible to apoptosis

HIV-specific CTLs kill CD4 cells

CD4 count gets low enough to start showing symptoms and opportunistic infections occur

AIDs = when cd4 cell count drops to 200 cells/microL and opportunistic infections
what are the receptors for HIV
CD4 AND either

CCR5 (macrophages, DC, and Tcells)
or
CXCR4 (on activated T cell)
how does HIV enter cells
gp120 and gp41 on viral surface bind CD4 and coreceptors

lipid bilayers merge and virus enters
discuss the function of the HIV enzymes:
integrase
protease
reverse transcriptase
integrase = integrates viral DNA into host DNA

protease = breaks lipid bilayer membrane so the virus can enter

reverse transcriptase = makes DNA from RNA, now have viral cDNA
how does activation of immune cells induce HIV viral production
after the virus gets into T cells, the T cell gets activated, NFkB binds and starts txn of RNA of HIB genome. transcripts can be used to make protein and some are packaged
discuss the function of rev and tat
genes activated in HIV life/infection

two pieces combine, and need splicing to get final product

transported to cytosol. tat will bind provirus and activate transcription
rev binds RNA transcript and has it migrate to cytosol

make proteins, synthesize birus, buds from cell, and then cell dies
how do some HIV therapeutic drugs work?
target HIV enzymes to inhibit viral assembly and mechanisms

infected cells die soon so HIV must continually infect new cell

AZT drug = NT analog, looks like a NT so reverse transcriptase thinks its a NT so it puts it in DNA BUT it infects human DNA

protease inhibitors
why is it difficult to get vaccines produced for HIV
high mutation rate

uncertainty over what type of immune system is necessary
Type I hypersensitivity
-how is it triggered
-which cell types are involved
-example of disease/symptoms it causes
classic allergy

IgE reaction

molecular type of Ags - proteins only induce t cell responses, low doses, low molecular weight, highly stable, highly soluble, contains peptides

TH2 cells deliver signals that allow B cells to proliferate and differentiate into IgE producing Plasma cells

Subcutaneous Ag (mast cell activation, increase vascular permeability leads to localized swelling)

allergic rhinitis (inhaled Ag enters mucosa and activates mucosal mast cells. blood vessel permeability and epithelium activation)

allergic asthma (mucosal mast cells capture Ag, inflammatory mediatiors contract smooth muscle, increase mucus secretion from airway epithelium and increase blood vessel permeability. mediated by cytokines and eosinophil products)

food (ingested) allergens - ingestion of Ag activates mucosal mast cells, activated mast cells release histamine which acts on epithelium, blood vessels, and smooth muscle
systemic anaphylaxis
drugs, serum, benoms, peanuts, shellfish

enters intravenously (either directly or after rapid absorption)
causes edema, increased vascular permeability everywhere, tracheal occlusion so cant breathe, circulatory collapse, and death

Ag in blood stream enters tissues and activates CT mast cells through out the body - mast cells degranulation and release of inflamatory cytokines
hygiene hypothesis
both genetic and environment cause

-high or low susceptibility
-grow up in hygenic envt versus growing up in un-hygenic envt

hygenic envt people are more susceptable to pathogens since youre not exposed to it as a child
type II hypersensitivities
ab mediated cell destruction via IgG or IgM

ABO mismatched blood transfusion can cuase it

reactions to certain Antibiotics can be type II
type III hypersensitivities
immune complex mediated

serum sickness - bit by snake/spider and go to hospital, give you Ab against the enom, horse Ab that you make a Ab to horse Ab - second exposure to same venom, all this Av you already have against horse venom, not going to clear them away quickly
type IV hypersensitivities
delayed type
mostly TH1 mediated
reaction to dyes, cosmetics, metals, poison, etc.
types of autoimmune diseases
organ specific AI diseases
systemic AI diseases
Hashimotos thyroiditis
auto-Ab's against thyroid Ags
cause tissue destruction by macrophage and auto-Ab's
hypothyroidism (not enough thyroid hormone) destruction and Ab's make it not work
autoimmune anemias
pernicious anemia - auto ab to intrinsic factor > low B12 uptake> low RBC

autoimmune hemolytic anemia - auto ab to RBC Ag, Abs bind to RBC's
good pastures syndrome
autoimmune ab to basement Ag (type IV callagen)

epithelial cells sit on basement membrane

auto-ab activates compliment and damage tissues (esp kidney and lungs)

compliment split products also cause inflammation
IDDM
insulin dependent diabetes mellitus type I

altoreactive CTLs that destroy Beta cells that make insulin

no insulin production
Graves disease
too much thyroid hormone

auto Ab to TSH

get an activated t cell that makes auto TSH
myasthenia gravis
antibodies that bind to ach receptor

receptors get endocytosed and degraded therefore you dont get muscle contraction eventually paralysis
SLE
systemic lupus erythematosus

auto Ab to a host of self Ag - make Abs to DNA or histones.

immune complex deposit - type II damage

higher amts of C5a - neutrophils aggregation and vasculitis
mutiple sclerosis
autoimmune responses against the myelin sheath of nerve cells

motor weakness, impaired vision, impaired coordination, paralysis

unknown trigger - cause local inflammation in CNS, BBB becomes permeable to leukocytes and blood proteins so that leukocytes get into the CNS

t cells specific for CNS ag get activated

destroy myelination
rheumatoid arthritis
Chronic inflammation of joints (other problems as well)
Auto-Ab (often IgM) is specific to IgG. IgG-IgM immune complexes form - Type III hypersensitivity
what are the major and minor histocompatibility antigens?
antigens that trigger transplantation rejection


Major histocompatibility antigen = MHC or human leukocyte antigen (HLA)
Polygenic: 3 genes (HLA-A, B, C) for class I, 3 genes (HLA-DP, DQ, DR) for class II
(Per haploid genome)
Polymorphic: many allelic variations in a population at each gene


Minor histocompatibility antigen - not one molecule but is any Ag that is different between two people. functionally the same but presentation of Ag is different
why do patients t cells recognize donors allogeneic mhc
only t cells can recognize your own mhc so how can they recognize a donor mhc?

no negative selection against the donors mhc

start with total t cell repertoire selected for MHCx.. ones that bind too strongly are negatively selected. some of the t cells will cross react with MHCw from someone else. if you get a donor with MHCz you will have t cells cross reacting with MHCz.
what are the methods of tissue typing? how do they work?
microcytotoxicity test
-take cells from recipient and from two potiential donors and then on a plate with lots of little wells. each column has an Ab for a different HLA allotype.. HLA-a for example. trying to match MHC II first.

mixed lymphocyte reaction - irradiate cells so they can no longer proliferate themselves, then mix donor and recipient lymphocytes measure t cell proliferation and t cell cytotoxicity
what are direct vs. indirect allorecognition?
direct - t cells are activated by donor DCs and then migrate to donor tissue to kill donor graft

indirect - donor tissue presents MHC.. donor mhc is picked up by recipient DCs, digested, and presented to t cells
what are the three different types of rejection?
hyper-acute rejection
acute rejection
chronic rejection
what are the drugs currently used for transplantation rejection?
corticosteroids - bind to steroid receptors and changes gene expression. turns on genes that have immune effects. reduce cytokine transcription, reduce enzyme production, and causes anti-inflammation

mitotic inhibitors - stops cells from proliferating, stop DNA replication, stop proliferation of all cells

FK506, cyclosporin, rapamycin - targets more specific factors like nfat... preventing t-lymphocyte activation.
what are some specific therapies (ab-mediated) in development for transplantation
anti-cd4 therapy and other mAb Therapy
mAb's are injected into people and they act as either blockers or depleters. deplete of APC in organ using anti-APC Ag Ab

CTLA4-Ig - if the t cells recognize graft Ags they become activated.. however, if you give CTLA4, T cells that recognize graft Ags lack co-stimulation and become anergic... bCTLA4 binds B7

anti-cd40 ligand -
hyper-acute rejection
recipient has to have pre-existing Ab to the donor molecules (mhc) already.. this person has seen the donors HLA before, form abs, so next encounter the Abs bind vasculature of donor, causing inflammation and cut off blood circulation to new organ and organ will be rejected

if you do not match the blood groups, then the person has ab's against this blood type
acute rejection
kidney will have APCs from the donor. once kidney is connected to recipient, apcs migrage out and they start activating recipient t cells.. effector t cells migrate to the graft and launch an immune response. graft gets destroyed by effector t cells
acute rejection
kidney will have APCs from the donor. once kidney is connected to recipient, apcs migrage out and they start activating recipient t cells.. effector t cells migrate to the graft and launch an immune response. graft gets destroyed by effector t cells
chronic rejection
happens when you have minor histocompatibility differences

alloantibodies recruit inflammatory cells to the bood vessel walls of the transplanted organ

increasing damage enables immune effectors to enter the tissue of the blood vessel wall and to inflict increasing damage
how is bone marrow transplantation done, and what is graft vs. host disease?
1. find bone marrow compatible match
2. pt undergoes irradiation and chemotherapy to get rid of their own immune cells
3. bone marrow infusion
4. stem cells will start hematopoiesis and are selected for the thymic epithelial cells
5. healthy patient

GVHD
when bone marrow is transplanted the t cells in the transplant attack the recipients tissues
why is it necessary to humanize abs for therapies
to avoid serum sickness

do so by making transgenic mice with human Ab genes
or by doing molecular sub-cloning of chimeric Ab
passive immunization
advantages and disadvantages
when you dont give a pathogen you give actual Abs usually when disease is mediated by toxins and when you need it to work really fast. either horse Abs or Human pooled abs

+ works fast and does clear away toxin

- not a lasting immune memory and if you need a second immunization you will have an immune response to the ab
active immunization
give a pathogen for people to "practice on"
what are three different types of active immunization vaccines
whole organism, purified molecule vaccines or DNA based vaccines
types of whole organism vaccines
live attenuated or killed
live attenuated vaccines
examples, +-
alive but modified like polio vaccine

BCG is the vaccine for TB,

+ is its really affective
-might turn virulent, contamination, storage is difficult
killed whole organism vaccine
examples, +-
killed with formaldehyde or heat

+ is that it wont turn virulent
- not alive so it floats around in system, not as effective, fails to kill all of it, process of killing might get rid of some Ags
types of pruified molecule vaccines
polysacchaide vaccine, toxoid vaccine, recombinant Ag vaccine
polysaccharide vaccine
examples, +-
carbohydrates of Ag is what the Ab binds to but need t cell help, need a protein presented by MHC therefore you give a protein linked to a polysaccharide called a toxoid

tetanus uses this linked recognition
toxoid vaccine
examples +_
have to be modified, just give toxins
recombinant Ag vaccine
first one was HepB
gene for Ag is cloned into yeast they make the protein, and you harvest it and give it as a vaccine
what are the DNA based vaccines
recombinant vector vaccine or DNA vaccine
recombinant vector vaccine
clone a gene in a plasmid, put it into a virus, thats the recombinant vector vaccine
DNA vaccine
clone a gene in a plasmid inject into muscle

+ is that DNA is very stable and can last a long time