Immuno Flashcards
(132 cards)
1
Q
Type 1 Hypersensitivity reaction
A
Immediate
allergic, med by IgE, mast cell med anaphylaxis
2
Q
Type 2 HS rxn
A
cytoxic, antibody-dependent
mediated by IgM and then IgG, directly targets antigens
3
Q
Type 3 HS rxn
A
immuno complex (ab/ag complex) (caused by aggregates of ab's in tissue)
4
Q
Type 4 HS rxn
A
delayed type, cell-mediated or ab-dep
causes granulomas, Th1 cells activate monocytes, cytotoxic T cells also do dmg
5
Q
Delayed type HS process
A
bug bite, DCs take up injected antigen, process and present in light zone of lymph node on MHC. Th2 cells with TCR get stim and clonally expand. Th cell interacts with antigen again in tissue, now can activate cytos. Eosinophils (via IL-5) also are brought in, producing cytos. 1-2 days
6
Q
What type of HS is TB test?
A
delayed
7
Q
What do Th1 cells interact w
A
B cells + others, pain/sickness
8
Q
What do Th2 cells interact w
A
Macros + allergic cells, for itch
9
Q
What do Th17 cells interact w
A
neutrophils
10
Q
What do Th1 cells form from?
A
IL-2
11
Q
What do Th2 cells form from?
A
IL-4
12
Q
What do Th17 cells form from
A
IL-6 and TGF-B
13
Q
What do Treg form from?
A
TGF-B only
14
Q
What types of pathogens do ____ respond to?
- Th1
- Th2
- Th17
A
Th1: viruses
Th2: helminths, ticks
Th17: bacteria
15
Q
Which immune cell can cause the most damage?
A
neutrophils!
16
Q
What happens in immediate HS?
A
- Antigen comes in, binds to and cross links IgE (pumped out by plasma cells) on Fc of mast cell, degran of preformed mediators and stim new mediators.
- serotinin/hist (vasc perm and bronchoconstr), tryptase, haprin, eicosanoids (PGD2 and LT C4), and cytokines (IL-4 and TNF)
- w/ no contact, neither immed or delayed HS, with some, delayed only, with more both, with many just immed (T cell anergy), and with very many neither (B cell anergy too)
17
Q
What do cytokines IL-4 and TNF do in immediate HS
A
IL-4 promote Th-2 cell formation, class switching in B cells, upreg MHC TNF is a pyrogen prod fever
18
Q
What causes the itch and edema?
A
edema from hist receptors on venules, itch from hist receptors on C fibers (unmyelinated nerves)
19
Q
Cytotoxic rxn process and autoimm disorders?
A
antibody such as IgG matches antigen and promotes complement activation, can do this with self such as in:
goodpastures, RF, autoimm hemo anemia
20
Q
Immune complex rxn (ag-ab rxn) process and disorders?
A
- ab:ag complex forms clumps that deposit in vessels and activ8 complement
- can be SxE from diph toxin serum tx
- SLE, RA, PSGN (kidneys)
21
Q
Most frequent example of immune complex HS autoimm disorder?
A
POST STREP GLOMERULO NEPHRITIS (deposits in kidneys)
22
Q
Delayed HS examples?
A
TB test, celiacs, IgA against self
23
Q
What do the following cause? IgM, IgG, IgA, IgE T-cells Killer T Th1, Th2, and Th17?
A
IgM and IgG complement activation IgA celiacs IgE immediate HS T cells delayed HS Killer T: autoimm Th1: PPD, Th2: allergic dermatitis, Th17: autoinflamm
24
Q
What HLA class do CD8 ad CD4 cells target?
A
CD8 targets HLA class I ABC CD4 targets cells with HLA class II D-PQR
25
Types of transplants (4)
autograft (same person)
iso (twin)
allo (diff person same species) (most transplants, want similar MHC I proteins to transplant donor)
xeno (diff species) (high rjxn)
26
First set primary vs second set secondary transplant rejection (for small grafts with vascular anastomosis)
1st: 10-20 d, type IV cytotoxic T-cell med HS
2ndary: <7d to recognize, based on immuno memo, white graft can occur, also CD8+
27
Most common allograft?
pregnancy!
28
What is direct vs indirect allorecognition?
Direct: DCs from DONOR present antigen on MHC, and host's T cells recognize this as foreign, causing immune resp against organ
Indirect: donor MHC prots is processed by host APCs (and are thus presented on host MHC) in spleen, causing rxn against organ
29
What are white grafts?
fast ab rxn against allograft, endoth binding/comple rxn/thrombosis cuts off blood flow to area leading to dead white tissue,
30
4 types of transplant rejection?
Hyperacute (min-hr), ab's have immed rxn to organ (tpe 2 HS) eg white graft, blood mismatch against donor blood/tissue
Accelerated rej: d, memo-T cells mount resp
Acute rej: d-w: prim activation of T cells, type 4 HS (T cells prod cytokines, alerts CD8 cells to kill), chronic inflam
Chronic rej: inevitable in transplants, delay with immunosuppressants, preformed ab's, immune complex Type 2/4, leads to interstitial fibrosis, indirect allorec
31
What meds can be used as immunosuppressants in transplants?
```
Corticosteroids
Azathioprine
Cyclosporin
Tacorlimus
Fingolimod
```
32
Corticosteroids
Corticosteroids (eg prednisone)- anti inflam suppr cytokine and macros(interferes with IFN-y)
33
Azathioprine
Azathioprine (coupled w above, decr purine syth/DNA synth in dividing T cells to bring down immune resp)
34
Cyclosporin and Tacrolimus
Cyclosporin: lowers IL-2 prod, lowers Th1 activity
Tacrolimus decr IL-2 gene promotor (decr IL2 and IL2R)
(initially inhibit calcineurin activity)
35
GVDH
Graft Vs. Host Disease:
DONOR cd8 cells react with host's APCs containing host self-antigen
-rel IL-2 and IFN-y
-rash, liver, GI, lung
-acute: all transplants, chronic can be months later
-collag depos, lesions, wasting, immunodef from auto-ab's
36
GVDH
Graft Vs. Host Disease:
DONOR cd8 cells react with host's APCs containing host self-antigen
-rel IL-2 and IFN-y
-rash, liver, GI, lung
-acute: all transplants, chronic can be months later
-collag depos, lesions, wasting, immunodef from auto-ab's
-can be antigen cross-presentation, where donor cells present recip pep fragments to both Th and CTLs
37
What cytokine do Th1 cells produce/ role?
IFN-y, Th1 plays role in cell mediated immunity
38
What cytokine do Th2 cells prod?
IL-4, humoral imm
39
What to Tregs express?
CD4 and CD25, made during (-) selection in T cell maturation
40
Positive vs negative sel in T cell maturation?
(+) T cells are tested to see if they can bind to self MHC and recognize as self
(-) Testing to see how tightly or loosely they bind to MHC/self-ag (dont want too tight of bind bc can be self reactive)
41
Main role of Treg (suppressor/regulatory T cells)?
peripheral homeostatic maintenance and prevention of autoimm (leave thymus and go to periph)
42
What do Treg produce to suppr immune resp?
| What do they decr?
IL-10
in placenta of mom to baby, but also suppress tumor cells
Treg decrease amount of IL-2 (affinity from CD25), Tregs soak it up like a sponge
43
IPEX sndrome
X linked immunodysreg from mutation of foxp3 (req for Treg differentiation to suppr immune resp, and prevents autoimm)
44
Immunologic tolerance
failure to mount resp to specific antigen
Deletional tolerance: usu self reactive T cells are deleted in thymus by (-) selection, but can escape
Regulatory tolerance: in thymus, Treg make IL-10 to suppr self reactive T cells in periph
45
Neonatal tolerance
exposure to maternal antigens
46
tolerogen
fetus becomes "tolerized" to maternal antigens, so antigens dont stim immune resp and are now called tolerogens
47
Central tolerance
clonal abortion/elim (clonal anergy/apop)
elim of self reactive cells (bind self MHC too tighly in eng selection), occurs in PRIMARY lymphoid organs, but if escape.....
48
Peripheral tolerance
Functional deletion, cells that dont prolif/diff in periph lymphoid organs (no co stim, no cyto prod)
49
What does T cell anergy occur from
deactivation due to lack of co-stimulation
50
How does CTLA-4 induce anergy?
(CTL)A-4 is expr in Treg, and upreg in activated T cells to modulate immunes resp
- if it binds to B7 if APC (instead of CD28) can turn off cell cycle
- drugs can block or activate CTLA-4
51
If self reactive T cells escape thymus, how can we prevent them from destroying cells
- sequestration; ag hidden from immune sys, barrier
- immunoprivileged site; sites in body that can tolerate ag without inflamm
- deletion; apoptosis/anergy by CTL4A
- immune regulation: Tregs secreting IL-10
52
Molec mimicry example
- antigen looks a lot like self antigens so immune sys makes ab's to self
- primary immune resp already occurring, eg strep pyogenes, where some B/T cells get stim and prolif when they shouldnt (self antigen), B CELL TOLERANCE is inactivation of autoantibodies
53
How does route of inoculation influence immune response
oral and IV are tolerant
| subcut, IM, and ID are immunogenic
54
What happens in antigen presistance
eg chronic viral infection overcomes immune sys bc of exhaustion
55
Diff between autoimmunity/autoreactivity and autoimm disease?
- autoimm: common, breakdown of self tolerance, rxn of lymphocytes against self antigens
- autoimm disease: less common, self-directed immune resp, assoc with primary event eg surgery infxn radiation
56
what is a neodeterminant
foreign ag binds to self ag, creating new ag and triggering autoimm
57
type of autoimm patho in RA
inflitration of T cells, incr cytokine prod (3 types) causing chronic inflam
58
What is ADCC
antibody dependent cellular cytotoxicity:
| abnormal if NK cells kill anything with ab bound to it (even if self)
59
4 types of autoimm diseases and what disease they cause
cell mediated- type 1 diabetes
cell/antibody mediated- RA
antibody/cell mediated- pern anemia
antibody mediated- lupus
60
4 types of autoimm diseases and fxns
- cell med: cell inflitrate from chronic inflam, incr in antigen pres and cytokine
- cell/ab med: infiltrates in joints, depos of immune complex in joints comple acitvation with neutro accum , tx with TNF-a inhibs
- ab/cell med: auto ab's against par cells and IF, chronic distruction of gastric mucosa so cant absorb b12
- ab-med: UV causes cross link dimers rec by b cells, makes autoab's against nuclear dna material and self reactive IgG attack skin, causing malar rash, immune complex deposition causing arthritis and glomeruloneph
61
Hyperacute rejection
immediate, within minutes to hours, involves ANTIBODIES against donor (type 2 antibody HS)
62
What does TGF-b do in chronic rejection
In chronic rejection, TGF-B induces interstitial fibrosis and smooth muscle proliferation.
63
What type of transplant does GVHD often occur from?
Bone marrow transplant! Since marrow has a lot of its own early T cells, CD4/8 cells from the GRAFT may attack the host tissue
64
Eradication vs Elimination of a vaccine?
Eradication: completely gone (dont need control method)
Elimination: gone in a certain area
65
What is an example of an ideal pathogen for vaccines?
| Impossible pathogen?
smallpox! one strain, no mutation, no carrier stage, short onset, get immunity fast, easy sx.
Another easy one is polio. only affects humans, can be controlled by good hygiene (fecal oral), virus has no envelope and limited ag's, herd immunity possible
Impossible is malaria: euk, mosquito and human hosts, animal transmission, genetic diversity and ag variation, diff ag's for each stage
66
Active vs Passive immunity?
Active- protection by persons own immune sys, permanent
| Passive- protection from another (temporary protection)
67
Homologous vs heterologous antibody
Homol: pooled human ab, human hyper-ig, both have ab's against many antigens
Heterol: synth or natural, eg HBAT (botulism) or 'mab for RSV
68
What does -mab indicate?
monoclonal antibody
69
Live attenuated vs Inactivated vaccine
Live atten: virus, bact, weakened form of wild virus/bact (works well, 1 dose)
Inactivated: via heat, chemicals, can be whole virus./bact or fractional (protein subunit or toxoid, and polysacc pure/conjugate)
Rule: The more similar the vaccine is to the pathogen, the better the immune response!
70
2 examples of toxoid inactivated vaccines?
C diph and tetanus
71
Pure polysacc disadv?
dont always work in kids and not long lasting bc no T cell inv, can improve by conjugating to others
72
Example of inactiv conjugated vaccine
H influenza
| also pneumo/meningococcus
73
Currently used bacterial vaccines
```
DTaP (diph, pertussis, tetanus)
HiB (h influenza B type)
meningococc/pneumococc
BCG
S typhi
```
74
What is an adjuvant
- substances that enhance resposne with vaccines (replace lost stuff in converted vaccine), delay clearnace or uptake, prolonging time APCs can present ag pieces
- They're dose sparing (reduce amt needed) and good for at risk pops and mucosa
- Example: ALUM (Intramuscular)
75
Main adjuvant used for humans?
Aluminum
76
What is the diff between primary and secondary immunodeficiency?
- Primary is congenital/hereditary
| - secondary is acquired
77
Diff between auto inflam, autoimmunity, and immunodeficiency?
- Autoinflammation: innate immune resp that won't stop
- Autoimmunity: adaptive immune resp that won't stop
- Immunodeficiency: immune resp that doesn't' start (most are ab deficiencies)
78
What are the top 3 predictors/warning signs of primary immune deficiencies?
Failure of infant to gain weight or grow
Need for IV antibiotics to clear infections
Family history of primary immunodef
79
Fungal infections can occur with defect in which imune cells?
What about viruses?
Bacteria?
Fungal: T cells and phagos
Viral: T/B
Bacterial: B (antibodies), complement, and phagos (esp encapsulated bacteria)
80
What are 3 diseases casued by antibody prod defects?
X linked agammaglobulinemia aka Brutons
IgA def
Hyper IgM syndrome
81
What is baby missing if born premature?
IgG, bc transfer happens from mom to baby in 3rd trim (after birth prod own IgG)
82
```
X-linked agammaglobulinemia (Bruton's tyrosine kinase deficiency)
Defect
Pop
Sx
Lab smear
Tx
```
Defect in Btk (for B cell activ/diff)
Seen in babies
Otitis media, pneumonia early
Small or no tonsils/lymph nodes bc lack B cells
Normal lymph count, so T cells, but NO B cells
Tx IVIG (intravenous immunoglobulin)
83
Selective IgA Deficiency
Lab
Sx
Incr risk for
IgA lvl less than 10 mg
Recurrent sinopulm infxn and autoimm/GI/endocrine
At risk for CVID
84
```
Hyper IgM syndrome (CD40L deficiency)
Genetics
Def
Sx
Lab
Tx
```
X linked
CD40 ligand def (not CD4 interaxn with B cell) so no costim, no proper B cell diff or class switching, so stuck w/ IgM
Sx: pre school boy PNEUMOCYSTIS PNEUMONIA with otitis media, tubes, fevers, always on antibiotics, mouth ulcers
Lab has high IgM low others
Tx IVIG, unless diagnosed early where u do MARROW TRANSPLANT
85
If child has pneumocystis pneumonia what might this indicate?
Has Hyper IgG (esp if boy) or HIV
86
2 impt phagocytic defect immune diseases?
Leukocyte adhesion defect
| Chronic granulmatous disease
87
Chronic Granulomatous Disease
Inheritance
susceptibility
X linked
Defect in NADPH dep oxidase, usually can get over this by using other ROS, but if bacteria is catalase positive then this H2O2 will be broken down so still wont work
Thus CGD patients are sus to catalase positive stuff like S aureus, Serratia, nocardia, and aspergillus
88
CGD again
Hallmarks and sx
Dx
Tx
-young kids
-recurrent staph/pneum infxn
skin and organ abcesses ("cold" staph abcesses dont make pus), and recurrent fungal infxn
-Tx: antibiotic and antifungal prophylaxis (prevention) with trimehto sulf (bactrim), maybe IFN injxn
89
3 types of SCID
X linked
ADA/PNP (purine)
Autosomal
90
SCID hallmarks
failure to thrive, diarrhea, thrush, recurrent infxn, low CBC
91
X linked SCID
Gamma chain deficiency so dysfuxn in IL cytokines, prevents growht of B and T cells (so no lymphoctyes)
Tx with gene therapy or bone tarnsplant
92
ADA or PNP SCID
nucleotide breakdown issue, so accum of nucleotide precursors which are toxic to developing lymphocytes (no B/T cells)
Tx: enzyme replacement
93
In flow cytometry, which cells should we look at first to ID issue with immune sys?
First look at T cells, then B, then NK
94
What is a common T cell def disease?
DiGeorges
95
```
DiGeorges
mech
sx
dx
tx
```
22q11 deletion, 3rd/4th pharyngeal pouches fail to develop, NO thymus/parathyroids
Sx: dysmorphic or small face, not enough Ca, less T cells bc no thyumus, congenital heart disease, early in life like seizures murmurs etc
Dx via CXR (shadow in anterior mediastinum where thymus should be)
Tx: thymic transplant (but still dev delay)
96
Primary immune def common sx?
```
resp/sinus infxn
no tonsils
enlarged lymph nodes
failure to thrive
skin lesions
candidiasis
diarrhea
(HIV and CVID present later in life)
```
97
```
CVID (common variable immunodeficiency)
Pop
Def
Sx
Dx
```
Late onset hyogammaglobulinemia
Primary
Can have onset age 20 or 30
Decline in all Igs
Recurrent bacterial sinopulm infxns, GI/endo/hemo issues, weight loss, diarrhea, chronic productive cough, fevers
HIV TEST NEGATIVE and Ig's still NORMAL
BRONCHIATASIS in CXR (lung tissue pockets, airway scarring)
98
Tests for inherited immunodeficiencies (primary much more rare than acquired)
Check for serum Ig (abnormal in most indivs)
Check for ab resp to vaccine or blood group ag's
CBC for wbc count
Flow cytometry and FACS (fluor) to look for specific lymphos (T cells CD3/4/8, NK CD56, B cells CD19)
Check for delayed type HS
NBT/chemilum
Compl activity with CH50
HIV testing
Check for comon thigns like allergies celiacs and CF
99
Tx for ab def?
gammaglobulin
100
Tx for complement issue?
give plasma w complement
101
Tx for phagocyte problems?
G-CSF to increase neutros, prophylactic antibios, IFN-y in CGD
***SEE CHART!
102
Autosomal SCID
defect in Rag/JAK so cant VDJ recomb, no B or T cells
103
How does giving periodic boosters help
clonal expansion and aff maturation (protection is larger and more specific)
104
Which vaccines are live attenuated?
```
MMR (measles mumps rubella)
Varicella (chicken pox)
[Oral polio]
[Nasal influenza]
[Rotavirus]
```
105
What do live vaccines do
- live viruses grown in non human cells, mutations or delete virulence gene
- v potent cell mediated and humoral resp
106
Killed/inactivated vaccine example
Injected polio
107
Subunit vaccine (incl toxoids)
DTaP, hep B, acellular pertussis, Hib, conj penumococ
| all use capsular polysac conj to carrier prot
108
What are examples of types of immunosuppressive drugs?
- Antihistamines (antagonists of H1 receptors that block histamine from binding thats already been released from mast cells)
- Leukotriene modifiers (block rel of LTs)
- NSAIDS (cox inhiits, block conv of ARA into PGs and LTs)
- Global immunosuppressive drugs (corticosteroids like prednisone/olone, anti-prolif drugs like azathioprine, methotrexate, and inhibs of T-cell activation like cyclosporin A, tacrolimus)
109
5 pro-inflammatory cytokines
```
TNF-a
IFN-y
IL-1
IL-2
IL-8
Can be blocked by drugs to decr inflam
```
110
What does IL-1B do in immunomodulation?
Stimulates IL-6 prod which causes fever (activ lymphos in vasc endoth, tissue dmg)
111
What does TNF-a do in immunomodulation?
SHOCK!
From changing vasc perm too much
fever
112
Monoclonal antibody nomenclature
"Mab"
"mu" murine (mouse)
"zu" humanized (v little mouse, best)
"xi" chimeric (lots of mouse)
113
What is AIT and what is the mech?
Allergen immunotherapy desnsitization, increase allergen from small amt til person makes own Tregs (made from IL-10) to downreg IgE
-down reg Th2 so less IL-4 thus less IgE
Upreg Th1 so more IFN-y and IgG to overwhelm IgE and prevent it binding
-Peanut oral desensitization transient, small GI risk, patch less effective for adults, no injections run anymore
114
Cells involved in immune resp for asthma/ allergies
If pollen
Make IgE to pollen, binds to mast cells, if exposed IgE x links on mast cells causing degran, hist and TNF-a rel causing sneezing/itching, LTs and PGs cause wheezing/bronchoconstr, IL-4/IL-12 cause mucus and eosinophil recruitment
-Also Th2 CD4 T cells prod IL-4/13, leading to prod of IgE, IL-5 recruits eosinophils
115
What is Omalizumab
humanized monoclonal Ab
-Binds circulating IgE at Fc receptor site, preventing the IgE from binding mast cells (IgE omal complex not rec by complement), cleared
116
Immunomodulation therapy for RA, and 3 mechs?
RA is mix of adaptive and innate immune sys causing destruction and erosion of joints
Target main tissue destruction cytokines IL1/6/TNF-a
-block w/ anti-TNF-a drugs like eten
-anti-CD20 drugs (block too much RF on B cells by blocking CD20, but SxE is decr serum Igs)
-JAK3 inhibis (block dna TFs for cytokine rel)
117
JIA (Juvenile Arthritis)
Sx?
Tx?
warm swollen joints in knees, wrist, can't run as fast, stiffness, usu not painful
-Tx: NSAIDS/oral steroids, then methotrexate, or can try anti TNF drugs
118
```
SoJIA (Systemic Juvenlie Arthritis)
pop
mech
sx
dx
tx
```
- subgroup of JIA, boys and girls
- INNATE immune sys driven
- Fever, rash (salmon on pale skin and pink on dark skin), trunk/extrem, fleeting/changing, hepsplen/lymph/cardi/pleuritis
- correlated with elevated IL-6 (can measure) and IL-1
119
SoJIA Tx?
anti IL-1 receptor blocker (IL 1 rec drives prod of IL6), OR
| CTLA-4 Ig to interrupt CD28-B7 co stim between T and APCs (CTLA4 binds to B7/CD80 on APCs so T-cell CD28 cant bind)
120
Immunomodulation Tx for Chron's
Sx
Tx
Incr in Th2 cells in intestine mucus
Ulcers and cobblestoning (swelling peyers patches), abd pain and poor digestion
-Tx: Block cytokines such as TNF, probiotics (inhib VFs, upreg IL-10 and TGF-B), helminthic tx (to activate Treg, but would need a every few weeks)
121
Addl ImmunoTx?
```
Plasmaphoresis (remove bad plasma or exchange w good)
IVIG replacement (replace Ig's)
Specific Igs (eg synagis, give IgG injxn to infants with RSV as if from mother)
Cancer tx: knock out tumor cells, or change T cell receptors
```
122
What makes cancer cancerous?
Cells dont have as many reqs for growth factors (grows independently of GFs eg hela cells)
Loss of anchorage dependence aka cells can be made in any tissue
Can grow all over each other like zombies
123
What does VEG-F do in cancer?
VEG-F stimulates angiogenesis in cancer cells, giving nutrients to tumor, which can metastesize
Cacner is dangerous bc is has self-cells so hard for immune system to mount proper response/ hard to destroy
124
What general processes occur during cancer formation?
Mutation in tumor suppressor gene so inactivated allowing cells to prolif, mtuation in proto-oncogene creates oncogene, mutation, more tumors suppr genes inactivated causing cancer
-Genes, env, viruses, and bacteria can stim cancer growth
125
How can you immunize a mouse to a tumor>?
By injecting it with irradiated tumor cells
126
What can a tumor vaccine involve and why are they difficult to implement>?
too many diff strains of tumors, and only works if given before tumor cells are formed so cant rly use prophylactic measures
127
What cells are involved in innate response to tumors?
NK cells attack tumor cells bc lack MHC I (primary innate resp)
Macros help a bit by making cytos like TNFa, and O2/N2 cpds
128
What cells are involved in adaptive response to tumors?
CD8 T cells are the main attackers of tumors
CD4 also help by making cytos
Antibodies only impt in oncogenic viruses
129
What is concomitant immunity?
situation where antigen immunity in one part of body prevents growth of cells with that antigen (eg immunity to tumor at second location but unable to mount immunity at primary tumor site)
130
What are 5 ways in which tumors can evade immune recognition?
- Low immunogenicity: dont expr MHC, costim (so tolerated, maybe anergy of T cells)
- Antigenic modulation: tumor cells can endocytose ab-ag complex and degrade it
- Tumor-induced immune suppression: Tumor cells secr factors that inhib T cell resp, such as TGFb and IL-10, and induce Tregs
- Tumor-induced privileged sites: tumor makes physical barrier that tells body its a privileged site so no adaptive immune resp
- Immunoediting: tumor cells dev anti-immune responses via selection/variants//resistance and survive
131
Immunotherapy for tumors:
- specific vaccines
- cytokine therapy
- passive immunotherapy
- Specific vaccines: dendritic cells with spec tumor ag to activate CD8 resp, vaccines w/ plasmids whcih have tumor ag, IL-2, GM-CSF
- Cytokine tx (give cytos that stim immune sys like IL-2! can also give others)
- Passive immunotx: amplify anti-tumor cells (isolate and propogate via IL2)
132
Immunotherapy for tumors:
- antitumor monoclonal ab's
- anti t-cell mabs
- Antitumor mabs: abs bind to tumor with specific ag, initiating ADCC (ab dep cellular cytotox), eg NK cells, ab's can be bound to toxin or radioactive nucleotide to kill tumor (targeted tx that relies on specificity of immune sys
- Anti T-cell mabs: block CTLA4 which normally downreg T-cells, so is now active again (anti-CTLA-4 antibody keeps T-cells alive to kill tumor)
