Exam 1 Spring Flashcards
what is the most effective method for preventing infections?
vaccination
what is the 4th modality of ca tx?
immunotherapy
what is the reason immune med diseases are rising?
unknown
innate immunity definition
def in place before infection –> rapidly respond
limit infection before adaptive imm response
adaptive immunity
shaped by exposure
incr magnitude and def cap with each successive exposure to partic microbe
features of innate immunity (6)
- epith barries
- present from birth
- in place prior to infections –> responds rapidly
- activated by structures shared by diff classes of microbes
- no memory - not any faster 2nd exposure
- trigger and amp adaptive imm response
features of adaptive immunity (3)
- patho-sp
- memory! enhanced by repeated exposure
- uses cells/mol of innate imm sys to elim microbes
cell meds of innate AND adaptive are derived from….
pluripotent hemtopoietic stem cells in bone marrow
- lymphoid stem = adaptive
- myeloid stem = innate
neutrophil morphology
muiltilobed nuc
small pink granules
short-lived
fx neutrophils
phago
activ bac-cidal mech
monocyte morphology
bean-shaped nuc
CD14 positive
fx monocyte
phago
recruit to sites of inflamm
differn –> tiss macrop
macrophage morph
in tissues
ruffled memb
cytop: vacuoles and vesicles
CD14 positive
fx macrophage
phago microbes and dead cells
secr cytokines
APC
dendritic cell morph
found in epith tissues
long cytop arms
fx dendritic cells
antigen
- capture
- txp
- present
mast cell morph
found in tissues, mucosa, epith
small nuc
cytop packed with large blue granules
fx of mast cells
release granules (histamine) during allergy, anti-helminth
eosinophil morph
found in bloodstream, some epith
bilobed nuc
LARGE pink granules
fx eosinophils
kill ANTIBODY-COATED parasites
basophil
found in bloodstream
biloced nuc
LARGE blue granules
fx basophils
nonphago
release active sub during allergy
NK cells morph
found in: lymphoid, bloodstream
CD16, 56
LARGE cytop granules
fx NK
kill
- tumor
- virus
- ab-coated target cells (ADCC)
lymphocyte morph
found in: bloodstream, lymph nodes, submucosa, epith
LARGE dark nuc
small rim of cytop
fx lymphocytes
B: CD 19, 20, 21 - produce Ab
TH: CD 3, 4 - reg imm responses
CTL: CD 3, 8 - kill infected, altered cells
plasma cell
found in: lymph nodes, spleen, MALT, bone marrow
small dark nuc - intense staining GOLGI
end cell of b-lymphocyte differentiation
fx plasma cell
prod Ab
types of adative immunity
humoral
- bloack infections
- elim extracel microbes
cellular
- elim phago microbes
- kill infected cells
- elim resevoirs of infection
humoral immunity is med by:
Ab made by B cells
- secr –> circ/lumens of mucosal organs –> bind extracel microbes/toxins –> neutralization (prev int-act with host tissues)
cell-med immunity is med by:
T cells aga INTRA-cell microbes
A previously health 8 year old boy is infected with an upper respiratory tract virus for the first time. During the first few hours of infection, which one of the following events occurs?
A.A lymphocyte response rapidly controls the infection.
B.An immune response dominated by neutrophils and monocytes keeps the infection under control
C.Killer CD8 T cells destroy infected epithelial cells
D.Antibody neutralizes the virus and prevents the spread of infection
E.Memory B cells quickly become activated to secrete antibody
A.An immune response dominated by neutrophils and monocytes keeps the infection under control
foreign sub recog by B and T lympho are called…
antigens (epitope recog)
diff b/w how B and T cells recog antigens?
T = ONLY protein
B/antibodies: MANY types
what are naive lymphocytes?
B and T lympho not yet encountered antigen
“immun” inexperienced - inactivated state
protective imm aga microb induced by…
host T and B cell recog AND response to foreign antigen
what kinds of indiv are said to be “immune”
when lympho have responded to microbe antigens and protected from subseq exposures of THAT microbe
active immunity is when…
protection from prev recog microbe
induced by exposure to foreign antigen
what is passive immunity?
immune WITHOUT exposure NOR response to that antigen
how to confer passive immunity?
txf serum or lympho of sp-imm indiv
fxs of innate and adaptive immunity are med by…
cytokines
- soluble proteins/peptides
- concep sim to horm
- pleiotrophic: may have 2(+) unrelated effects
in normal indiv, primary infection is cleared by…
BOTH innate and adaptive immunity
A standard treatment of animal bite victimes, when there is a possibility that the animal was infected with the rabies virus, is administration of human immunoglobulin preparations containing anti-rabies virus antibodies. Which type of immunity would be established by this treatment
A.Active humoral immunity
B.Passive humoral immunity
C.Active cell-mediated immunity
D.Passive cell-mediated immunity
E.Innate immunity
Passive humoral immunity
key features of adaptive imm sys (7)
- specificity
- diversity
- memory
- clonal expansion - inccr # antigen-sp lymphoctytes faced with microbes
- specialization - gen repsonse optimal for def aga diff types of microbes
- contracftion/homeostasis
- nonreactive to self
specificity means
only clones of cells with approp receptors to recog a PARTICULAR antigen becomes activated
antigens that adaptive imm sys can recog is…
virtually limitless due to extremely diverse repretoire of antigen receptors
what is the downside of having such a diverse repertoire?
cells cap of recog 1 antigen fairly small –> clonal expansion of CURRENT infection
effect of clonal expansion after infection clears?
adaptive response declines (contracts) but MEMORY cells remain
- rapid more exhanced response of microbe return
At 15 months of age, a child received a measles-mumps-rubella (MMR) vaccine. At age 22, she is living with a family in Mexico that has not been vaccinated and she is exposed to measles. Despite the exposure, she does not become infected. Which of the following properties of the adaptive immune system is illustrated in this scenario?
A.Self Tolerance
B.Diversity
C.Specialization
D.Memory
E.Specificity
Memory
Is it a B cell or a T cell mophologically?
NO DIFFERENCE!
All lymphocytes are morphologically similar
How to tell diff lymphocytes apart?
CD - detect using antibodies
most common method used to detect presence of bound Ab is
flow cytometry
B cell CD expr
19
20
21
T cells CD expr
2
3
subsets:
- CD 4
- CD 8
NK cell CD expr
16
56
BCR
receptor that recog antigen
memb form of antibody
how to B cells med humoral immunity?
prod Ab aga EXTRACELL patho/toxins via recog soluble antigens and antigens pres on microbe surf
antigen recognition and T/B cell activation results in…
effector cells
effector cells of B cells =
plasma cells –> secr Ab
- antigen recog induced differen B cell –> plasma –> prod soluble Ab with SAME sp as memb-bound Ag receptor
Ab combat extracel pathogens by…
neut –> prev infection
facil destruction –> phago or complement
Activated effector B cell (Plasma cell)
notice
- LOTS of cytop
- LOTS mito
- LOTS RER
How do T cells defect antigens?
INTRACELL
recog small frag of antigen that have been broken down and presented by APC
Steps to Ag presentation?
- APC capture Ags
- brkdown into small frag
- present on MHC
- recog by TCR (T-cell antigen receptor) on T cell
- activation T cell
- cell med immunity
examples of APCs
dentritic cells
macrophages
activated B cells
Th cells: antigen recog and effective fx
recog microbial antigen on APC –>
- activate macrophages
- inflam
- activ prolif and diffen of T and B cells
cytotoxic T cells: antigen recog and effector fxs
recog infected cell expressing microb antigen –> KILL
fx of regulatory T cells
what are their CDs?
SUPRESS immune response
CD4 and CD 25
when lymphocytes emerge from bone marrow or thymus….
they are mature but first must find antigen recog by their receptors
- circ from blood –> peripheral organs (1 round a day)
B cell deficiency presentation
absent/reduced follicles/germ centers in lymph organs
reduced serum Ig lvls
result:
- pyogenic bac infections
- enteric bac/viral infections
T cell deficiency presentation
reduced T cell zones in lymophoid organs
reudced DTH rxns to common antigens
defective T cell prolif responses to mitogens IN VITRO
result:
- viral/intracell infections: p. jiroveci, atyp mycobac, fungi
- virus-assoc malig: EBV lymphomas
what are the most important APCS? Why?
dendritic cells (DCs)
reside in tissues most commonly used as portal of entry of pathos
- skin
- muc tissues
A 2 year old boy is evaluated for a immunodeficiency disease. He appears to have a normal number of CD3+ cells, however, there are no CD19+ cells found in the blood or peripheral lymphoid organs (spleen, lymph nodes). Which of the following cell types is this boy deficient in?
A.B cells
B.CD4 T cells
C.CD8 T cells
D.NK cells
E.Neutrophils
B cells
Consider the 2 year old boy in the previous case found to be deficient in CD19+ cells. Which of the following capabilities would this child’s immune system lack?
A.The presentation of antigen by MHC molecules
B.The recognition of antigen derived from an intracellular pathogen
C.The mobilization of neutrophils during the first few hours of an infection
D.The production of antibody against extracellular pathogens
E.The maintenance of the epithelial barrier
production of antibody against extracellular pathogens
1st line of defense of the immune sys
- skin
- muc memb/secr
- normal flora
2nd line of defense
- innate immune cells
- inflam
- complement
- antimicobe substances
3rd line of defence
adative immunity: lymphocytes
intraepith T cells
final protective cmpt of epith
non-classical T cells – expr only limited range of antigen receptors
cell mediators of innate immune sys (6)
NENEMI
neutrophils
epith
NK cells
eosinophils
monocytes/macrop
ILC (innate lymphoid cells)
soluble mediators of innate immune sys (4)
- complement
- cytokines
- acute phase reactants
- coag factors
biological barriers of innate immune sys
normal flora
most patho gain entry to tissues via
skin
respir tract
GIT
fx of normal flora of epith
competes for nut and oclonization
sstim secr antimicrobial sub
epith mechanical barriers
tight jxns
mucus (goblet cells) - prevent adherence
mucociliary elevator
epith chem barriers and mechanism
skin
- sweat - anti-microbe FA
muc memb
- HCl (parietal cells) - low pH
- tears/saliva - enz dig
- defensins/cathelicidins - direct toxicity
- surfantant - opsonin
PAMPS
limited # of microbial products recog by innate immune sys that are shared among broad groups of microbes
- structures essential for surv and infectiveness of microbes
NOT pres on host cells
PAMP of influenza/mumps/parainfluenze/measles
ssRNA
types of receptors of innate immunity
TLR
N-formyl peptide
mannose
scavenger
recog of PAMPS med by…
PRR (pattern recog receptors)
- TLR = major family
- NLR (nod-like) = nicrobial prod, dmg tissues
- RIG-like = viral RNA
- c-type lectin = recog mannose residues
types of TLRs
- bac lipopep
- bac pipopep/peptidoglycan
- dsRNA
- LPS
- bac flagellin
- bac lipopeptides
- ssRNA
- ssRNA
- CpG DNA
PAMP/DAMP of NOD-like receptors
bac cell wall pep-glycans
intracel crystals
changes in ATP/ion conc
cytosolic DNA sensors recog what kinds of PAMP/DAMP
AIM2
- bac and viral DNA
c-type lectin receptors recog
mannose
- microbial mannose and fructose residues
dectin
- fungal cell wall glucans
scavenger receptors recog
CD36
- microbial diacylglycerides
innate immune receptors med
- prod of effector molecules/cytokines –> induce innate and adaptive immunity
- stim phago
- chemotactic –> guide phago to infection site
NLRP-3 engagement results in…
combine with caspase 1 –> activates IL-1 –> fever, inflammation
complex = inflammasome (NLRP-3 + caspase 1)
sterile (non-infectious) inflam NLRP3 activators
gout: monosodium urate
alz: beta-amyloid plaq
DM2: free FA, islet amyloid polypep
atherosclerosis: ox-LDL, cholesterol
MyD88 deficiency
recurr, severse pus-forming/pyogenic bac infection
IRAK4 deficiency
recurr severe bac infections
- cellulitis
- arthritis
- meningitis
- osteomyelitis
- organ abscesses
- sepsis
UNC93B deficiency and TLR3 mutations
incr suscep to encephalitis caused by HSV
IKK/NEMO deficiency
ectodermal dysplasia
- conical/absent teeth
- sparse hair
- hypohidrosis (decreased sweat glands)
immunodefic
- recurr sinopulm infections
- mycobac
- opportunisitic org
Carl is a 1 month old healthy child who has not, as yet, received any childhood vaccines. He presents with his first episode of otitis media that is successfully treated with antibiotics. Which of the following immune components contributed the most to the clearing of the infectious agent during the first few days of the infection?
●
A.Antigen receptors on B lymphocytes
B.Toll like receptors on macrophages
C.Cytokines that promote antibody production
D.T cell responses to bacterial antigens
E.Memory B cells
TLRs on macrophages
what cells are sentinels for infectious org?
resident DCs and tissue macrophages
recog of PAMPS/DAMPS by resident tissues macrophages results in…
release of inflam cytokines: IL-1, TNF-alpha
- stim P and E selectin
- rolling of neutrophils due to shear forces and weak bonding
after rolling, what happens to neutrophils?
activated macrophages prod chemokines (IL-8/CXCL8) –> induce HIGH AFFINITY integrins (ICAM-1, VCAM-1)
- neutrophil recog IL-8 receptor via their CXCR 1 & 2
- neutrophils bind to integrins via their Mac-1, LFA-1, VLA-4
how to neutrophils extravasate?
b/w endothelial cells: increased basc perm via histamine, PG, LT
G-CSF
granulocyte CSF
- prod @ site of infection
- incrs prod of neutrophils by bone marrow
inflammation is …
accum leukocytes @ infection site
assoc vasc dila
incr leakage of fl/proteins into tissue
hallmark of acute inflamm
neutrophils
temporally distinct patterns of expr of adhesion mol/chemokines typ result in…
early neutrophil recruit
- LFA1/MAC-1 : ICAM-1
- CXCR1/2 : IL-8
later monocyte recruit
- VLA-4 : VCAM-1
- CCL2 : CCR2
leukocyte adhesion deficiency
auto recessive - decr mvmt leukocytes to inflam
- delated sep of umbilical cord
- recurr bac/fung infections: skin, lungs, GIT, perirectal
absent/deficient
- β2 integrins, LFA-1 and Mac-1: heterodimers of CD18 & 11
result:
- prev tigh adhesions
dx and tx of leukocyte adhesion deficiency
dx: CD18 flow cytometry
tx: BMT/SCT
It is generally thought that a limited amount of inflammation at the site of vaccination helps to stimulate a strong adaptive immune response to the vaccine antigens. Which of the following substances, if introduced with the vaccine, would best serve the purpose of attracting a neutrophil infiltrate into the area?
A.G-CSF
B.IL-8
C.Prostaglandin
D.E selectin
E.TNFalpha
IL-8
what are the most abundant leukocyte in blood?
neutrophils
neutrophil granules
specific: lysozyme, collagenase, elastase - degrade bacterial
azurophillic: defensins/cathelicidins - microbicidal
NETs
DNA chromatin networks –> trap bac/fungi –> kill via its granules
what is the prominent emch by which inflammation can dmg host tissue?
neutrophil granule enz and ROS
prod and storage of neutrophils
lifespan?
prod: G-CSF
reserve pool in bone marrow
lifespan = 6 hours : major cmpt of pus
macrophages orgin from
fetal hematopoietic organs (yolk, sac, liver)
fx macrophages (4)
- ingest/kill microbes and apop host cells
- secr cytokines –> onto endothelial cells –> recruit leukocytes
- APC –> (+) T cells
- prom repair of dmg tiss
once a microbe has be engulfed by a macrophage…
killed by phagolysosome
- ROS: NADPH oxidase/MPO
- iNOS
- proteolytic enz (lysozyme)
CGD
mutation in NADPH phagocyte oxidase
effect:
- recurr infection with catalase –> bac/fungi infections
- granulomas: inab to kill/phago bac
M1
classically activated macrophages - inflam/kill via innate inflam response
cytokines secr by M1
IL-1beta: vasc-endo & lymphocytes, local tiss destruction, effector cells –> fever, prod IL-6
IL-6: fever, acute-phase proteins by hepatocytes
IL-12: activ NK cells
TNF-alpha: increase vasc perm, incr lymph drainage –> fever, shock
CXCL8: recruit neutrophils, basophils
M2
activated by IL-4 & IL-13 in absence of strong TLR signals –> reduce inflammation & med tissue repair
what are the link b/w innate and adaptive immunity?
DCs: capture antigen –> bring to draining lymph nodes –> present to naive T cells
types of dendritic cells
cDC (conventional) - capture antigen in perip –> present to adaptive imm in draining lymph nodes
pDC (plasmacytoid) - circ in blood –> recruit to inflamm sites –> activated –> prod IF-1 (interferon 1)
mast cell released things and timing: (3)
degranulation - seconds
eicosanoids - minutes
cytokines/chemokines/ GFs - hours
mast cell degranulations and fx
histamine - vasodil, increase perm
TNF-alpha
tryptase/chymase - proteolytic –> kill bac & inactiv toxins
amines
mast cell eicosanoids
LT
PG
cytokines/chemokines/GFs of mast cells
TNF-alpha, IL-4/5/6/13/17, VEGF
true or false: NK cells express antigen receptors
FALSE - no antigen receptors like T and B cells
how do NK cells recog target cells?
absence of MHC I
“stress signals”
how do NK cells induce apop of target cells?
perforin/granzyme
Fas/FasL
NK cell receptors: inhib v activating
inhib:
- KIR: bind MHC I
- KLRG-1
- NKG2/CD94
activating:
- CD16 (FcR) - ADCC (Ab-dep cell-med cytotoxicity): kill Ab-coated cell
- NKG2D
NK cell cytokines
IL-12: prod INF-gammy
IL-15: dev/mat
IF-1: enhance killing fx
what fxs together to kill intracell microbes?
activated macrophages prod IL-12 –> activ NK to –> IFN-gamma –> activ macrophages
viruses and the immune sys
- Virus infects host cells
- CD8 T cells recognize viral antigen:MHC complex. Kill host cell
- Viruses evolve to evade the CD8 T cell response by suppressing MHC class I expression
- Natural killer cells develop to recognize cells that have decreased MHC class I expression
- Viruses encode decoy MHC class I molecules that cannot present Ag, but suppress NK cell activation!
Lymphocytes with Limited Antigen Receptor Diversity
features of both innate and adaptive immune sys: considered part of innate sys
- gamma-delta T cells: somatically rearrange Ag recept
- NK-T cells: T-cell antigen receptors (TCRs)
- B-1 cells: expr Ag receptors, secr Ab (usually prod natural Ab that recog carbs on cell walls of bac)
- marginal zone B cells: Ag receptors
main functions of complement
3 pathways of complement activation
classic: IgG/IgM Ab - humoral adaptive immunity
alt: microbal surf proteins - innate
lectin: lectin mannose binding - innate, but requires time gain strength
C3 cleavage
central to all C’ pathways:
- later in classic/lectin
- activates alt
a - chemoattractant: mast cells –> vasoactive
b - opsonin (coval binding)
activation of alt C’ pathway
C3 spont hydrolyzed in plasma in low lvls –> iC3 (C3 tickover)
fac B (serine protease, active enq of C3/C5 convertases) + iC3 –> C3b –> readily bind to microbe surf
- cleavge of fac B by fac D
- stby by properdin
–> activation alt path
C’ lectin pathway
MBL - acute phase reactant (liver) during periods of inflamm
- innate immunity: bc init by microbial prod
bind MBL to microbe –> bkdwn C4 & C2 –>
- C4b + C2a –> complex –> C3 convertase
- C3b binds complex –> C5 convertase
- init late steps of C’
- C3b binds complex –> C5 convertase
C’ classic pathway
init by bindning Ab to Ag: adaptive
- C1 bind to Fc portions of 2 IgG or IgM –> cleave C4 & C2 –> C4b2b complex = C3 convertase
- C3b binds to complex –> C5 convertase
all 3 C’ pathways lead to…
coat of convalently attached C3b = opsonin
last steps of C’
C5 convertase cleaves C5
remaining C6-C9 bind seq to C5b
C9 polymerizes –> MAC –> pokes hole
C’ deficiencies
C3: recurr severe bac infections –> usually fatal
C5-C9: incr suscept to Neisseria (thin cell wall - esp suscep to MAC)
regulation of C’
mammal cells can reg, microbes cannot
- overwhelming C’ –> coat with antibody –> C’ target
Factor I
proteolytically cleaves C3b and C4b
Factor H
dissoc alt pathway C3 convertase
co-fac for Fac I med cleavage of C3b
C4BP
dissoc classic C3 convertase
co-fac for Fac I med cleavage of C4b
DAF
dissoc c3 convertase
CD59
blocks C9 binding –> inhib MAC
MCP
membrane cofactor protein
cofac for Fac I for proteolysis of C3b into inactive frag
C1 INH
stops activation of classic path: interferes with C1q cmpt
- prev C1 r2s2 from activating
hereditary angioedema
inherited: deficiency in C1 INH
* excessive C1 activation –> subseq activation of kinin sys (C2b)
unpredictable/recurr episodes of periodic swell in subQ/submuc
in the innate immune response, the principal sources of cytokines are…
macrophages
mast cells
dendritic cells
major proinflamm cytokines
TNF
IL-1
IL-6
local effects of proinflam cytokines
vaso-dil: marginalization of leukocytes
activates endothelium - adhesion mol
incr vasc perm - diapedesis/extravasation
sys effects of inflam cytokines
liver: acute-phase proteins –> C’, opsonin
bone marrow, endothelium: neutrophil mob –> phago
hypoT: incr body temp –> decr microbe replication
fat/M: get more E –> decr microbe replication
pyrogens
ab to induce fever: IL-1, IL-6, TNF-alpha
elev temp
- slows patho growth: most grow & replic optimally @ temps below human body
- actively seques iron –> lim bac growth
acute-phase proteins
IL-6
- MBL –< incr phago, trigger lectin C’
- CRP - binds PL-choline –> incr phago, trigger classic C’
- SAA
early clinicla and patho manifestations of septic shock are caused by…
very high levels TNF-alpha due to systemic bac infection
IL-8
recruits neutrophils
IL-12
prod by activated macrophages and DCs –> NK & CD4 T cells –> IFN-gama –> bidirectional activation
major innate cytokine prod in response to viral infection is…
IFN-I
- host cells recog via viral PAMPS (dsRNA) by PRRs (Rig-1)
secr by virally infected cells and leukocytes to protect surr cells from infection
- activ JAK-STAT sig pathway
fnal role of innate immune response
alert adaptive immune response
- signal 1: antigen recog by lymphocytes
- signal 2: moles induced during innate imm response
evasion of innate imm: pneumococci
cap polysacc –> inhib phago
evasion of innate immunity: staphylococci
produces catalase –> resists ROS
evasion of innate immunity: neisseria meningitidis, streptococci
sialic acid –> inhib C3/C5 convertase
M protein –> blocks C3 fx
resists alt C’
evasion of innate immunity: pseudomonas
synth mod LPS –> resists antimicrobial peptides
bone marrow
common lymphoid progen cell
- precursor: T, B, NK
- most steps B cell mat in BM –> finals events @ 2ndary lymphoid organs, particularly spleen
common myeloid progen cell
- RBCs, platelets, granulocytes (N, E, B), monocytes (most DCs)
thymus
3rd parayngeal pouch
- flat, bilobed
- 2 compartments:
- outer cortex = thymocytes
- inner medulla = T cell maturation
- DCs and macrophages help with mat
thymic cortical epith cells
secr IL-7: GF req for early T cell dev
thymic medullary epith cells
remove self-reactive T cells
thymus through time
enlarges during childhood
involutes after puberty
DiGeorge syndrome
mutations in genes for thymus dev
- T cell deficiency
also effects parathyroid & heart dev due to 3rd pharyngeal pouch origin
- hypocalcemia
•A 52 year old man who receives radiation therapy and cytotoxic drugs for treatment of cancer sustains significant damage to his bone marrow. Which of the following changes will most likely occur?
•
A.Decreased production of monocytes but not B lymphocytes
B.Decreased production of B lymphocytes but not T lymphocytes
C.Decreased production of neutrophils and monocytes but not B lymphocytes
D.Decreased production of B and T lymphocytes, monocytes, neutrophils, and red blood cells
E.Normal production of all red blood cells due to compensatory extra medullary hematopoiesi
A.Decreased production of B and T lymphocytes, monocytes, neutrophils, and red blood cells
•In DiGeorge syndrome, the thymus fails to develop. Which of the following characterizes the immunodeficiency state in this syndrome?
A.Low numbers of neutrophils and monocytes in the blood.
B.Deficiency in antibody production in response to bacteria polysaccharides
C.Deficiency in cell mediated immunity in response to an intracellular infection
D.Normal T cell numbers, however, defective T cell activation
E.Deficiency in B cell maturation
A.Deficiency in cell mediated immunity in response to an intracellular infection
peripheral lymphoid organs fx
collect/cencentrate antigens –> gives oppor for naive lymphocytes to recog
lymph contains (3)
debris from dying cells
antigens
DCs with captured antigen
celephantiasis
interstitial fluid collected by not drained by lymph
paracortical area of lymph node
DCs present captured Ags to T cell