Hdm Week 12

Front 1

extracellular bacterial infections: most important factor =

Back 1

adhesion

Front 2

if bacteria don't adhere to epithelium, they don't:

Back 2

infect

Front 3

"epithelial surface" =

Back 3

skin or lining of gut

Front 4

first solutionto adhering bacteria:

Back 4

slough off the epithelial cells

Front 5

if unable to slough, solution to adhering bacteria =

Back 5

Innate Immunity

- macrophages and neutrophils phagocytose the bact.

Front 6

**neutorphils are WAY better at ________________ than macrophages**

Back 6

phagocytosis

Front 7

if the innate immunity response is efficient, AI is not

Back 7

necessary

Front 8

if InnImm is not effective at killing bacteria, the bacteria will continue to proliferate, =>

Back 8

more bacterial load, for longer

= AI is necessary

Front 9

(normal infection => inflammatory signals =>

Back 9

WBC's called in)

**inflammatory signals are critical for survival**

Front 10

**what do extracellular toxigenic bacteria do?**

Back 10

**actually kill neutrophils**

Front 11

example of extracellular toxigenic bacterium =

Back 11

B. pertussis

Front 12

solution to extracell. toxigenic bact = AI, via:

(2)

Back 12

1. B cells + T helper cells become plasma cells and release AB's

2. memory cells combat reinfection

Front 13

**how do AB's combat bacterial toxin?**

Back 13

they **neutralize** the toxin, allowing macrophages and neutrophils to phag. the bact. wherever they've spread (over epithelium or within the cells at that point)

Front 14

Paradigm 1 of immunity: the AI __________ the InnImm

Back 14

*recruits*

Front 15

**vaccine =

Back 15

inactivated bact/viral toxing, antigen, etc

- used to create memory cells that then combat reinfection

Front 16

3 kinds of bact. that grow in the interstitium (between cells):

Back 16

1. capsular bact.

2. invasive bact.

3. bact. that prevent inflammation

Front 17

capsular bacteria:

(2)

Back 17

1. grow in interstitium

2. capsule makes them resistant to pahgocytosis

Front 18

response to capsule of capsular bacteria =

Back 18

Complement opsonizing

Front 19

what does opsonosis do to capsular bacteria?

Back 19

makes it easier for neutrophils to phag.

Front 20

why is Complement not an ideal response?

Back 20

b/c Complement is part of the II and therefore general

Front 21

AI opsonization is better b/c:

Back 21

it's specific to that antigen

Front 22

Paradigm 2 of immunity: the AI =

Back 22

the InnImm x 10

Front 23

3 examples where AI is 10 times more powerful than II:

Back 23

1. opsonization

2. neutrophil influx (for invasive bact.)

3. macrophage priming/optimization

Front 24

deficiency in opsonization =>

Back 24

susceptibility to *encapsulated* bact.

Front 25

example of invasive toxigenic bact:

Back 25

Staph aureus

Front 26

what does an invasive bacterium's toxin do?

Back 26

**takes out neutrophils in the surrounding area (in the interstitium)

Front 27

despite losing lots of neutrophils to the invasive toxin, the InnImm still:

Back 27

*prevents the spread* of infection

- allows AI to kick in

Front 28

it normally takes the AI _________ to kick in

Back 28

7 days

Front 29

**what's the AI response to invasive toxigenic bact?**

(2)

Back 29

1. AB's (which neutralize the toxin)

2. Th17

Front 30

what does Th17 do for invasive toxigenic bact. infections?

Back 30

**sustains/boosts neutrophil influx**

- brings in WAY more neutrophils than the II can

Front 31

what's the worst kind of bacterial infection?

Back 31

on in which the bacteria **prevent** the inflammatory signal from being released by infected cells

- tells neutrophils, "go away, we're good here"

Front 32

**what does no inflammation signal mean?**

Back 32

**bact. replicate unchecked

=> 50% mortality rate

Front 33

best example of bact. that prevent the inflammation signal =

Back 33

Yersinia pestis

(aka the plague)

Front 34

the plague ~

Back 34

a complete lack of II response

Front 35

with a normal inflammation signal, the II would still be able to:

Back 35

keep the bacteria in check as AI booted up, even if the II wasn't strong enough to overcome the bact.

Front 36

***early inflammation, particularly via neutrophils, is critical to:***

Back 36

hold the line until the AI comes in

Front 37

chronic granulomatous disease =

Back 37

NO ROS from neutrophls/macrophages => cannot kill bacteria

=> EVERY bacterium becomes a plague

Front 38

2 kinds of intracellular bacterial infections:

Back 38

1. cytosolic

2. vasicular

Front 39

best example of cytosolic bact. infection =

Back 39

Listeria mono

Front 40

cystolic bact. infection:

(4)

Back 40

1. bact. replicate *within* epithelial cells, to avoid detection

2. spread to the next one over, instead of releasing itself to the outside

3. not common

4. eventually replicate too much => can't avoid detection any longer => II discovers infected cell, phag's it

Front 41

defenses against cytosolic bacterial infections:

(4)

Back 41

1. autophagy (just swallow it, within the cell)

2. infected cells release cytokines that call up the II
(=> macrophages/neutrophils are there when infected cells blows up)

3. CTL's

4. Th1's (to upgrade/prime macrophages)

Front 42

the cytosol is actually _________________ to bacteria

Back 42

inhospitable

Front 43

vesicular intracellular bact. infections, like cytosolic, also:

Back 43

replicate within/spread from cell to cell

Front 44

***some intracellular bact. infections have macrophage subversion, which means:***

Back 44

the ability to infect a macrophage and use it to grow, instead of being phag'd by it

=> MORE bact. released

Front 45

soln to intracellular bact. infections = the AI, via:

(2)

Back 45

1. Th1 cells

2. AB targeting to neutralize and hold the bact.

Front 46

what do Th1 cells do for intracellular bact. infections?

Back 46

they release IFN-y

=> primes macrophages to combat subversion, by becoming **as good** at phagocytosing as neutrophils

Front 47

why aren't macrophages normally as good at phagocytosing as neutrophils?

Back 47

they would harm tissue via ROS

Front 48

upgraded macrophages are less likely to get taken over because:

Back 48

they are better at killing bact now

Front 49

tuberculoid leprosy ~

Back 49

too strong Th1

Front 50

fungal infections:

(2)

Back 50

1. fungi like cooler environments

2. hard to clear

Front 51

if extracellular, fungal infections are killed by:

Back 51

neutrophils

- a neutrophil influx is caused by Th17

Front 52

intracellular vacuolar fungi can ALSO take over:

Back 52

macrophages

- also combated by Th1 priming via IFN-y

Front 53

with parasites, chronic infection is very:

Back 53

common

Front 54

worms trigger:

Back 54

Th2 cells => B cells make IgE => IgE calls up mast cells, which call up eosinophils

=> eosinophils dog-pile the worm and release their toxic granules

Front 55

aberrant Th2 response ~

(2)

Back 55

allergy and asthma

Front 56

viral infections are, by definition:

Back 56

intracellular, and cytosolic

Front 57

viruses have STRONG anti-__________ abilities

Back 57

InnImm

Front 58

4 defenses against viruses:

Back 58

1. anti-viral proteins

2. NK's

3. CTL's

4. AB's (to mop up and bind viruses after CTL's are done, preventing them from entering cells)

Front 59

anti-viral proteins are made by:

Back 59

the infected cell,

following type 1 IFN signalling

Front 60

NK's are general, and so are not:

Back 60

as effective as CTL's

Front 61

viruses attempt to antagonize:

Back 61

EVERY step of the immune response, including MHC at every point

Front 62

viruses, bacteria, and parasites use a trick called:

Back 62

AB escape

Front 63

AB escape ~~

Back 63

creating new surface epitopes

Front 64

HIV makes new epitopes ___________

Back 64

weekly

=> continual evasion of AB's

Front 65

HIV also takes out ALL types of:

Back 65

CD4+ cells

Front 66

danger level 1 infection:

Back 66

toxigenic bacteria on epithelial surfaces

Front 67

danger level 2 infection:

Back 67

toxigenic *invasive* bact., within the interstitium

Front 68

danger level 3 infection:

Back 68

bact. that *prevent inflammatory signal*, also in the interstitium

Front 69

goal of vaccines is to prevent:

Back 69

*disease,*

not prevent infection

Front 70

most vaccines produce:

Back 70

AB's

Front 71

3 factors triggered by vaccines:

Back 71

1. AB's

2. CD8+ cells

3. CD4+ cells

Front 72

***what do Ab's do?***

(4)

Back 72

1. opsonize

2. neutralize

3. enhance phag. by macrophages/meutrophils

4. activate Complement cascade

Front 73

vaccines are presented by:

Back 73

MHC,

just like they do antigens

Front 74

why are germinal center B cells critical for effective AB response?

Back 74

B cells activated by antigen outside the germinal centers are **short-lived** and **cannot make memory cells**

Front 75

light zone =

Back 75

follicular dc's presenting antigen to B cells, which are then activated by nearby T cell helpers

Front 76

dark zone =

Back 76

rapidly-dividing, *activated* B cells

Front 77

somatic hypermutation occurs:

Back 77

when the B cells are prolif/diff. in the dark zone

Front 78

**long-living plasma cells colonize the:

Back 78

bone marrow, releasing their AB's to blood over years

Front 79

***long-living memory cells from germinal centers DON'T NEED:***

Back 79

T cell help to be activated

Front 80

adjuvants =

Back 80

mlcls added to vaccines in order to trick the immune system into seeing an infection and **activating the II**

which activates the AI

Front 81

the InnImm system is critical for:

Back 81

activating the AI

Front 82

**protein** antigens by themselves are poor:**

Back 82

vaccines, b/c they don't activate the InnImm very well

=> **need adjuvants**

Front 83

polysaccharide antigens stimulate:

Back 83

**T-independent** AB response

Front 84

why do polysaccharide antigens only stimulate T-INDependent AB responses?

Back 84

**b/c T cells can only recognize **peptides**

Front 85

polysaccharide antigens are poor vaccines b/c:

(3)

Back 85

1. don't cause germ. center rxn

2. innefficient class switching

3. NO B memory cells produced

Front 86

why are polysaccharide vaccines necessary?

Back 86

many pathogens have a **polysaccharide capsule**

Front 87

solution to poor immune response to polysaccharides =

Back 87

add protein adjuvant that links to polysaccharide vaccine

=> T-dependent response

=> **called a conjugate vaccine**

Front 88

conjugate vaccine =

Back 88

polysaccharide vaccine with protein adjuvant

(T-dependent response)

Front 89

the very young and the very old have limited:

Back 89

AB responses to polysaccharides and proteins

Front 90

primary immunodeficiency =

Back 90

**genetic** mutation

that messes up any step of the immune response

Front 91

primary immunodeficiency =>

Back 91

great susceptibility to infections, autoimmunity, and sometimes malignancy

Front 92

inheritance of primary immdef's is:

Back 92

AD, AR or X-linked

Front 93

primary immdef's are most readily spotted in:

Back 93

childhood

Front 94

most PID's are:

Back 94

**AB deficiencies**

Front 95

4 kinds of secondary immdef's:

Back 95

1. HIV

2. Trauma

3. nephrotic syndromes

4. intestinal lymphangiectasia

Front 96

nephrotic syndromes ~

Back 96

loss of factors like Ig and Complement

Front 97

intestinal lymphangiectasia =

Back 97

loss of lymph, with its Ig's and lymphocytes, into the gut

Front 98

***3 categories of immunodeficiency:***

Back 98

1. Humoral

2. Cellular/Combined

3. Innate Immune def's

Front 99

humoral immunity ~

(2)

Back 99

AB's and Complement

Front 100

humoral immunity:

(3)

Back 100

1. most common kind

2. ~frequent pyogenic infections

3. ~ chronic diarrhea

Front 101

diagnosing immdef's: think:

(2)

Back 101

quantity and quality

(what are they doing, or not doing)

Front 102

"pyogenic" ~

Back 102

inflammation and pus, usually due to bacteria

Front 103

AB's and Complement work in:

Back 103

concert

Front 104

hereditary angioedema is the result of a deficiency in:

Back 104

**Complement** C1 esterase inhibitor

Front 105

hereditary angioedema =

Back 105

massive swelling of face *wihtout* itching or hives

(NOT an allergy - no itching)

Front 106

6 specific AB (and thus humoral) deficiencies:

Back 106

1. XLA

2. Hyper IgM Syndrome

3. IgA deficiency

4. CVID

5. Specific AB deficiency

6. Transient Hypogammaglobulinemia of infancy

Front 107

XLA stands for:

Back 107

X-linked Agammaglobulinemia

Front 108

in XLA, the germinal centers are:

Back 108

**defective**

Front 109

result of defective germinal centers =

Back 109

defects in B cell maturation

- specifically, BTK of pre-B cell doesn't work => no maturation

Front 110

no maturation of B cells =>

(2)

Back 110

1. lack of AB's and B memory cells

2. underdveloped tonsils, Peyer's patches, spleen, and lymph nodes

Front 111

XLA:

(3)

Back 111

1. common in boys (duh)

2. B cells < 2% of lymphocytes

3. *normal* T cell # and func

Front 112

Hyper IgM Syndrome =

Back 112

normal number of B cells, but disproportionate expression of IgM vs. the other classes

Front 113

Hyper IgM is the result of:

Back 113

impaired class switching, via 2 mechanisms

Front 114

2 mechanisms of impaired class switching in Hyper IgM:

Back 114

1. defective signal to induce class switching

2. defective machinery to make the class switching happen

Front 115

what's the most common form of defective signaling in impaired class switching?

Back 115

bad CD40L

- it's X-linked

(bad CD40 ~ AR)

Front 116

IgA deficiency:

(3)

Back 116

1. most common immdef

2. usually asymptomatic

3. undetectable amounts of IgA

Front 117

CVID stands for:

Back 117

Common Variable Immuno Deficiency

Front 118

CVID:

(4)

Back 118

1. most common PID in adults

2. ~ reduced IgG, IgA, and/or IgM in serum

3. => absent or impaired specific AB response to previous infections/vaccines

4. => recurrent infections (so life-threatening)

Front 119

CVID results in an increased risk of:

(4)

Back 119

1. granulomatous diseases,

2. autoimmune disorders

3. splenomegaly

4. certain malignancies

Front 120

Specific AB deficiency =

Back 120

impaired AB response to **encapsulated* bact.

(and thus to polysaccharide vaccines)

Front 121

Spcific AB deficiency:

(3)

Back 121

1. recurrent sinopulmonary infections

2. normal B cell number

3. normal T cell number and function

Front 122

one NEEDS ________ AND __________ to take down encapsulated bacteria

Back 122

AB's

and

Complement

Front 123

transient hypogammaglobulinemia of infancy =

Back 123

delay in maturation of T helper cells for AB production

=> recurrent sinopulmonary infections

Front 124

onset of transient hypogammaglob. =

Back 124

6 months

- resolved by age 4

Front 125

IgG does a lot of:

Back 125

things

Front 126

lack of NK's =>

Back 126

increased susceptibility to Herpes virus family

Front 127

cellular immdef's ~

Back 127

**lack of T cells**

Front 128

Cellular ImmDef's are often called "Combined ImmDef's" because:

Back 128

a lack of T cells means a lack of T helpers which means a lack of B cell activation

Front 129

(CD4+ cells enhance:

Back 129

CD8+'s, NK's, and macrophages)

- and of course activate B cells

Front 130

clinical characteristics of T cell dysfunction:

(5)

Back 130

1. recurrent **intracellular** infections

2 **thrush** (classic)

3. failure to thrive (esp. due to diarrhea)

4. eczemous rash

5. anergy to antigens

Front 131

which pathogens grow intracellularly?

(4)

Back 131

viruses, some bact, fungi, and protozoa

Front 132

5 different Combined immdef's:

Back 132

1. SCID

2. DiGeorge Syndrome

3. Bare Lymphocyte Syndrome type II

4. Wiskott Aldrich Syndrome

5. Hyper IgE (Job's Syndrome)

Front 133

SCID =

Back 133

profound deficiency of T cells

=> NO AI

Front 134

why does SCID occur?

Back 134

B and T cells need some of the same proteins to mature

(e.g. ADA or RAG)

- lack of one of these prot's messes with both lines

Front 135

DiGeorge Syndrome =

Back 135

smaller or absent thymus

Front 136

DiGeorge Syndrome is the result of:

Back 136

defective development of 3rd and 4th pharyngeal pouch

Front 137

DiGeorge Syndrome is diagnosed immediately by:

Back 137

the absence of a thymic shadow on X-ray

Front 138

clinical features of DiGeorge Syndrome:

(4)

Back 138

1. depressed T cell immunity

2. dysmorphic face

3. hypocalcemia (due to lack of PTH)

4. congenital heart disease

Front 139

***DiGeorge is either:

Back 139

hypoplastic (partial)

or

aplastic (complete DiGeorge)

Front 140

***features of partial DiGeroge:***

(6)

Back 140

1. more common

2. +Hassell's corpuscles

3. **normal thymic function**

4. T cell function is adequate

5. B cells normal

6. usually free of infections

Front 141

***features of complete DiGeorge:***

(3)

Back 141

1. NO thymus

2. very few CD4+ cells

3. AB response is decreased

Front 142

Bare Lymphocyte Syndrome, type II =

Back 142

defective expression of class II MHC

= AR disease that looks like SCID

Front 143

BLS type II:

(3)

Back 143

1. impaired T cell activation

2. impaired maturation of CD4+ cells

3. normal/elevated CD8+

Front 144

Wiskott Aldrich Syndrome has 3 symptoms:

Back 144

1. eczema

2. thrombocytopenia

3. immunodeficiency

Front 145

thrombocytopenia =

Back 145

deficiency of platelets in the blood

Front 146

what causes Wiskott Aldrich Syndrome?

Back 146

defective WASProtein

Front 147

WASp ~

Back 147

actin polymerization

Front 148

Hyper IgE:

(4)

Back 148

1. severe eczema

2. cold abscesses

3. patients have retained primary teeth

4. high IgE

Front 149

Job's Syndrome is due to impaired function of:

Back 149

Th17 cells

Front 150

3 types of Innate Immdef's:

Back 150

1. chronic granulomatous disease

2. leukocyte adhesion deficiency

3. TLR deficiencies

Front 151

Chronic Granulomatous Disease =

Back 151

recurrent bacterial infections due to impaired ability of macrophages and neutrophils

Front 152

CGD:

(3)

Back 152

1. granulomas of skin, liver, lungs, lymph nodes

2. problems with wound healing

3. diagnosed with flow cytometry

Front 153

which immune cells specialize in wound healing?

Back 153

neutrophils

Front 154

in CGD, phagocytotic cells are able to ingest the bact. but not:

Back 154

kill it

- can't produce the necessary ROS burst

Front 155

leaukocyte adhesion deficiency =

Back 155

neutropils can't migrate or adhere

=> can't get to infected tissue

Front 156

LAD is diagnosed by:

(2)

Back 156

1. delayed umbilical cord separation

2. crazy-high WBC count but NO PUS

Front 157

diagnosing immdef's:

(3)

Back 157

1. growth chart

2. onset of symptoms

3. palpate lymph nodes

Front 158

as a result of no T cells to activate B cells, humoral immunity is impaired in:

Back 158

combined immdef's

Front 159

tolerance =

Back 159

not responding to self-antigens

Front 160

central tolerance ~

(2)

Back 160

bone marrow and thymus

Front 161

***what is responsible for addressing autoreactive cells that don't apoptose or anergize?***

Back 161

**regulatory T cells**

Front 162

what's one condition that results from a failure of central tolerance?

Back 162

Autoimmune Polyglandular Syndrome (APS1)

Front 163

APS1 is the result of a defect in:

Back 163

AIRE, which normally drives elimination of autoreactive cells

(automimmune regulator mlcl)

Front 164

3 mechanisms of peripheral tolerance:

Back 164

1. anergy

2. suppression by regulatory T cells

3. apoptosis

Front 165

anergy of autoreactive cells is achieved by:

Back 165

**blocking signal 2**

Front 166

apoptosis of autoreactive cells is achieved by:

(2)

Back 166

1. expression of pro-apoptotic prot's

2. death receptors

(both of them => caspases => apoptosis

Front 167

IPEX is an autoimmune disease that results from a failure to:

Back 167

suppress autoreactive cells via regulatory T cells

Front 168

ALPS stands for:

Back 168

Autoimmune Lymphproliferative Syndrome

Front 169

ALPS =

Back 169

uncontrolled expansion of potentially harmful autoreactive lymphocytes

Front 170

both B and T cells can be:

Back 170

autoreactive

Front 171

central B cell tolerance takes 2 forms:

Back 171

central deletion;

receptor editing

Front 172

breakdowns in tolerance =>

(2)

Back 172

autoimmunity or hypersensitivity

Front 173

breakdowns in tolerance occur due to:

Back 173

nature and nurture

Front 174

hypersensitivity =

Back 174

immune rxns that cause damage to the *body*

(rather than a pathogen)

Front 175

Type I hypersensitivity is actually:

Back 175

allergy

- IgE-mediated

Front 176

"allergy" = B cells make IgE =>

Back 176

IgE attaches to IgE r's on mast cells => r's form crosslink and bind antigen => mast cell is activated => release of histamine and recruitment of other WBC's to site (i.e. inflammation)

Front 177

allergic rxns generally happen within:

Back 177

5 to 10 minutes of exposure

Front 178

***allergies always cause:***

Back 178

itching

(due to histamine)

Front 179

3 forms of allergic rxn:

Back 179

1. atopic (quick) dermatitis

2. rhinitis

3. asthma

Front 180

atopic drmatitis usually occurs within:

Back 180

the first year of life

Front 181

rhinitis =

Back 181

inflammation of mucous membrane of nose

Front 182

anaphylaxis =

Back 182

sever allergic rxn

Front 183

anaphylaxis is the result of:

Back 183

massive amount of mast cells and basophils

=> massive amount of histamine

Front 184

anaphylaxis =>

(5)

Back 184

1. hives

2. flushing

3. airway constriction

4. drop in BP

5. vomiting

Front 185

50% of cases of anaphylaxis are caused by:

Back 185

food

Front 186

peanuts are dangerous b/c they're:

Back 186

heat resistant

Front 187

treatment of asthma comes in 2 forms:

Back 187

1. rescue via albuterol or xopenex (B-agonists)

2. control inflammaiton via steroids

Front 188

IgM ~

Back 188

first response

Front 189

IgD ~

Back 189

mature B cells

Front 190

IgG ~

Back 190

secondary response

Front 191

IgA ~

Back 191

protecting mucosa by preventing bacterial adherence

Front 192

IgE ~

Back 192

mast cells/basophils/inflammation

Front 193

Type II, III, and IV Hypersensitivity are all:

Back 193

**autoimmunity**

Front 194

Type II hypersensitivity =

Back 194

IgM or IgG **AB's act directly against tissue**

(via tissue self-antigens)

=> tissue damage

Front 195

3 types of Type II HS:

Back 195

1. Complement and Fcr' - mediated inflammation

2. opsonization and phag.

3. anti-tissue AB's

Front 196

anti-tissue AB's can damage tissue by either:

Back 196

activating r's OR inhibiting them

Front 197

Type III HS:

(2)

Back 197

1. AB-mediated

2. antigens can be either foreign OR self-antigens (tissue damage occurs either way)

Front 198

***difference between Type II and Type III HS =

Back 198

Type III makes deposits of **immune complexes** in tissues, esp. vessel walls

- the complex is the pathology

Front 199

**immune complex** =

Back 199

large, insoluble antigen-AB complex

Front 200

if an immune complex is deposited in vessels of the skin, it's called:

Back 200

vasculitis

Front 201

vasculitis:

(3)

Back 201

1. usually in small vessels

2. immune complex absorbs Complement => **low blood Complement levels**

3. ~ rashes

Front 202

classic example of Type III HS =

Back 202

Lupus

Front 203

**type III HS rxn to a FOREIGN antigen is called:**

Back 203

serum sickness

Front 204

symptoms of serum sickness =

(3)

Back 204

1. hives

2. fever

3. joint pain/stiffness

Front 205

serum sickness is the result of:

Back 205

medications, particularly high does of IV AB's

occurs couple weeks after administration, ends a couple of weeks after end of discontinuation

Front 206

one treatment of Type III HS is to decrease the immune response with:

Back 206

cytotoxic agents

Front 207

best drug to decrease immune response =

Back 207

Rituximab

Front 208

Rituximab:

(2)

Back 208

1. anti-CD20 agent

2. depletes autoreactive B cells

Front 209

(CD20 =

Back 209

r' on B cells)

Front 210

caveat with using Rituximab:

Back 210

it can give you secondary immdef due to depleting B cells

Front 211

Type IV HS has NOTHING to do with:

Back 211

**AB's**

Front 212

Type IV HS causes tissue injury via:

(2)

Back 212

1. CD4+ cells secreting cytokines => inflammation, activated macrophages

2. CD8+ cells directly injuring your cells


can be one or both of these at the same time

Front 213

in either case of Type IV mechanism, the damage is directed at:

Back 213

YOU,

not a pathogen

Front 214

common examples of Type IV HS:

(4)

Back 214

1. PPD test

2. contact dermatitis (including poison ivy)

3. MS (autoreactive against myelin prot's)

4. type 1 diabetes

Front 215

what's the predominant cause of cervical cancer?

Back 215

HPV

Front 216

immune surveillance =

Back 216

immune system's ability to protect against *spontaneous* tumor cell growth

Front 217

passive immunotherapy =

Back 217

transfer of cellular (T, NK, PMN) or humoral product that results in therapeutic response

Front 218

active immunotherapy =

Back 218

therapy that induces patient's own immune system to target microbe/tumor

Front 219

Phase 1 of clinical trials ~ prove that you're not:

Back 219

hurting anyone

Front 220

Phase 2 ~

Back 220

does it work?

Front 221

Phase 3 ~

Back 221

shows improvement to overall survival

Front 222

CD80/86 ~~

Back 222

B7/CD28

Front 223

CAR T cells stands for:

Back 223

Chimeric Antigen Receptor T cell

Front 224

CAR's are used to:

Back 224

target *circulating* tumor cells

Front 225

how do CAR's work?

Back 225

take the antigen-recognizing portion of an AB and engineer it with a T cell

=> bring T cell to the tumor

Front 226

CAR's ~~

Back 226

*active* immunotherapy

Front 227

cytokines are also used for immunotherapy; they are produced by:

Back 227

recombinant DNA technology

Front 228

3 examples of cytokines used in immunotherapy:

Back 228

1. interleukin 2

2. interferons

3. Granulocyte Stimulating Factors (GCSF)

Front 229

**what does anti-CTLA4 do?**

Back 229

blocks CTLA4 => blocks inhibition of T cells => T cells turn ON against tumor cells

Front 230

alloimmunity =

Back 230

immunity gained from an individual of the same species

e.g. fetus antigens gain immunity

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allograft =

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transfer of material between genetically non-identical individuals

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2 examples of allografts:

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1. blood transfusions

2. pregnancy

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autograft =

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transferring materials within the same individual

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isograft =

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transferring material between genetically similar individuals (i.e. twins)

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graft rejections are generally the result of:

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differences in MHC

(T cells are the primary rejector)

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allogeneic =

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immunologically dissimilar

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**GVHD stands for:

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graft vs. host disease

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GVHD =

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immune attack BY the transplanted cells against *the recipient*

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for HLA transplants, the more genetic mismatches you have, the more likely:

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your chance of GVHD

- aim to have no more than one mismatch

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what's the most significant problem with bone marrow transplants?

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GVHD

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GVHD is mitigated with:

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reduction of bone marrow T cells in the recipient

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3 phases of acute GVHD:

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1. Conditioning phase

2. Activating phase

3. Effector phase

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Activation phase =

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creation of Th1 cells out of donor T cells

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Effector phase of GVHD =

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tissue destruction by activated T cells' cytokines, etc.

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***solid organ transplants:***

(2)

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1. ***recipient vs donor***

2. e.g. ABO antigens of organ get recognized as foreign => hyperacute rejection (b/c antigens already existed to that bloodtype)

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***stem cell transplant:***

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***donor cells vs. recipient***

- T cells fight the new body they're in

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acute rejection takes:

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1 to 3 weeks

solid organ acute rejection => organ eventually dies

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in **acute rejection,** recipient's T cells can recognize allogenic HLA mlcls in one of two ways:

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1. directly

2. indirectly

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direct recognition of donor's HLA mlcls by T cells =

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recipient’s T cells recognize donor peptides b/c the *donor's* HLA presents them

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**indirect** recognition of donor's HLA mlcls by T cells =

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recipient's T cells recognize donor peptides once they've been processed by the recipient's APC's and are presented by the recipient's HLA

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chronic rejection takes:

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>21 days

- results in death of the graft

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Practically all transplant patients require immunosuppression regardless of the:

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HLA match

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critical time-frame for seeing if a graft takes is:

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2-4 weeks

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triple therapy of immunosupression before a graft:

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1. anti-inflammatories aka corticoids

2. DNA replication inhibitors

3. inhibitors of T cell activation (**cyclosporin/calneurin**)

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stem cell / "bone marrow" transplantation requires:

(3)

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1. HLA matching,

2. immune suppression of recipient

3. treatment of GVHD

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solid organ transplantation requires:

(3)

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1. ABO matching

2. immune suppression

3. monitoring of organs for chronic rejection (if acute rejection is averted)