Path 10: Diseases Of Immunity

Front 1

what is : ability of immune system to mount an antigen specific immune rxn?

Back 1

adaptive immunity

Front 2

what are the cells involved in adaptive immunity?

Back 2

T cells
B cells
antigen presenting cells
cytokines
macs/eosinophils/basophils/PMNs

Front 3

what's the humoral response?

Back 3

B lymphocytes make antibodies

Front 4

CD4 + T helper cells- make lots of cytokines = imp for : _________

Back 4

regulating mac and neutrophil activation; also help regulate B cell antibody production

Front 5

who does this: recog cells infected w/ endogenous viruses or mutated cells (cancer); imp in mediating viral clearance, intracellular pathogens like mycoplasma ?

Back 5

CD8 T cells

Front 6

are natural killers B or T?

Back 6

NEITHER!

Front 7

where do NK cells circulate?

Back 7

peripheral blood

Front 8

how do NK recognize cells?

Back 8

with IgG Fc receptor

Front 9

What cells do NK recognize and kill?

Back 9

IgG coated target cells : Type 2 hypersensitivity ADCC

Front 10

NK cells have an inhibitory receptor to recognize:

Back 10

MHC class I molecule

Front 11

what does the NK activating receptor recognize?

Back 11

stress proteins
viral proteins

Front 12

what are the tumor defense cells?

Back 12

NK cells

Front 13

what do NK T cells express?

Back 13

alpha/beta TCR and CD4 or CD8
NK cell markers

Front 14

how are CD4 NK-T cells polarized?

Back 14

Th1 or Th2

Front 15

what do the CD4 NK-T cells express?

Back 15

IFN-gamma
IL-4

Front 16

tumor cells downregulate __________ molecules to evade CD8

Back 16

MHC I

Front 17

what's this:
Via cell:cell contact and cytokine release, these T-cells function primarily through regulation of other effector cells: B-cells, Phagocytic cells?

Back 17

CD4+

Front 18

what's Lost in HIV?

Back 18

CD4+

Front 19

what are the different subsets of CD4+?

Back 19

Th1, Th2, Th17, Treg

Front 20

what Acts directly on infected or altered cells (e.g. viral infection and tumor surveillance). ??

Back 20

CD8+

Front 21

what cells are present at high numbers in mucosa of asthmatics?

Back 21

CD4+/Th2 NK-T cells

Front 22

what are general proinflammatory cytokines?

Back 22

IL-1, TNF-a

Front 23

what are general antiinflammatory/repair cytokines?

Back 23

TGF-b, IL-10

Front 24

what are cytokines that encourage proliferation?

Back 24

IL-2

Front 25

what are cytokines imp for differentiation?

Back 25

IL-7 (B-/T-cell maturation); IL-4 (Th2);
IL-12 (Th1); TGF-b & IL-23 (Th17)

Front 26

what activates endothelial cells, upregulate adhesion molecules so white cells go to areas of activation; activate liver to induce acute phase reactant proteins; induces febrile response ?

Back 26

TNF alpha

Front 27

what cytokines does Th1 lead to?

Back 27

IFN-g/IL-2/IL-12

Front 28

what cytokines does Th2 lead to?

Back 28

IL-4/5

Front 29

what cytokines does Th17 lead to?

Back 29

IL-17/chemokines

Front 30

what cytokine is associated w/ Cell mediated immunity effector cells (macrophages, NK cells)?

Back 30

IFN- gamma

Front 31

what cytokines are Humoral & IgE mediated effector cells (MAST cells, eosinophils) ass w/?

Back 31

IL-4, IL-5

Front 32

what are the steps in a B cell receptor growing up?

Back 32

Ig H & L chain = Signal 1

Variable region = Ag specificity

Signal 2 = Complement C3b binding

Front 33

Monoclonality in B cells is useful
clinically to demonstrate?

Back 33

neoplasia

Front 34

Variable region rearrangement and hypermutability of B cells(Both H & L chains) necessary for?

Back 34

1. Ag specificity
2. Ag binding to BCR
3. Hypermutability of variable region
4. Malignancy:

Front 35

Variable region rearrangement and hypermutability of B cells(Both H & L chains) necessary for Ag specificity?

Back 35

(e.g. cross reaction with self Ags would induce autoimmune disease)

Front 36

why is Variable region rearrangement and hypermutability (Both H & L chains) of b cell necessary for:Ag binding to BCR ?

Back 36

induces proliferation of B-cell; thus, selecting for B-cells with greatest BCR affinity to Ag

Front 37

why is Variable region rearrangement and hypermutability (Both H & L chains) of b cell necessary for:hypermutability ?

Back 37

Hypermutability of variable region (via RAG-mediated recombination) + Positive selection (#2 above) ensure “Affinity maturation” or continual production of Ab’s with greater affinity and specificity.

Front 38

why is Variable region rearrangement and hypermutability (Both H & L chains) of b cell necessary for:malignancy ?

Back 38

Malignancy: Monoclonal BCR clone rearrangement by molecular testing or monoclonal Ab production by electrophoresis.

Front 39

when does B cell receptor require double signal for activation?

Back 39

1. Coupling of BCR with Ag
2. Binding of CD21 with complement C3b

Front 40

what are the TCR heterodimers?

Back 40

alpha/beta (95%) and gamma/delta

Front 41

what is useful for immunophenotyping as T-cell
& T-cell subsets ?

Back 41

CD3, CD4, CD8

Front 42

Variable and constant region of TCR formed by _____________

Back 42

TCR somatic rearrangement

Front 43

monoclonality of T cells linked to :

Back 43

neoplasia

Front 44

T cell alpha/beta Co-express : ______________

Back 44

CD4 or CD8: Ag presentation MHC restricted

Front 45

T cell gamma/delta express:

Back 45

CD4/CD8 (-) or weak CD8: Targeted to mucosal / epidermal surfaces: Wound repair/tumor surveillance?

Front 46

Like the BCR, the TCR has a variable region responsible for

Back 46

Ag-specific activation.

Front 47

Again, like the BCR, the TCR undergoes a high rate of recombination events to

Back 47

generate Ag diversity.

Front 48

The presence of a monoclonal TCR population is an indication of a:

Back 48

T-cell neoplastic process.

Front 49

what is useful for: immunophenotyping or ID’ing T-cells in tissues or by flow cytometry.?

Back 49

The constant CD3 protein that is a part of the TCR complex

Front 50

CD4+ cells are responsive to Ag presented by :

Back 50

MHCII expressing APCs

Front 51

CD8+ cells are responsive to Ag presented by

Back 51

MHCI expressing cells.

Front 52

A secondary signal elicited by CD80 (B7.1) or CD86 (B7.2) binding to the T-cell CD28 receptor is necessary for________ and can lead to _________

Back 52

necessary for activation & can lead to anergy.

Front 53

Once activated, T-cells may express an inhibitory CD80/86 receptor called

Back 53

CTLA-4

Front 54

most of T cells are what type?

Back 54

CD4+ : 60%

Front 55

what are the First T cells activated by phagocytic cells of innate immunity.?

Back 55

CD4+

Front 56

MHC II mediates presentation of what?

Back 56

processed exogenous peptides (APC cells)

Front 57

what are the CD4+ Tcells a heterodimer of?

Back 57

a/b HLA-DP, DQ, DR proteins

Front 58

which T cells does HIV exhibit tropism for/take out?

Back 58

CD4+

Front 59

I Recognize endogenously synthesized
peptides in concert with MHC Class I (All nucleated cells): who am I?

Back 59

CD8+ T cells

Front 60

what are CD8+ T cells heterodimer?

Back 60

b-2 microglobulin + A, B, or C
HLA protein

Front 61

fun fact!

Back 61

b-2 microglobulin: hemodialysis associated amyloidosis

Front 62

what induces T cell lymphocyte prolif; in some tumor types like melanoma, give IL-2 to stim immune rxn against tumor?

Back 62

proliferative cytokines

Front 63

what is imp in regulating cell mediated immunity like macs and NK cells?

Back 63

IFN- gamma
*also induces normal nucleated cells to upregulate MHC I molecs so you get more effective CD8 cell mediate immunity

Front 64

ppl who are prone to allergies have more _________ and less _____________

Back 64

more IL-4 and much less of Th1 cytokines , interferon gamma

Front 65

may play imp role in reg chronic inflamm conditions like crohn’s or ulcerative colitis

Back 65

Th17

Front 66

what are the steps of B cell activation?

Back 66

when antigen binds to receptor, induces dimerization; if secondary signal w/ complement C3b binding to CD21 receptor will induce internalization and activation of B cell to make IgM (naive B cell)
IgM made during 1st time B cell introduced to antigen
also triggers MHCII upregulation.. B cell will present antigen to CD4 T cell that also recog antigen

Front 67

describe B cell activation for T cell independent antigens?

Back 67

(e.g. Pokeweed mitogen &
Carbohydrate antigens)
Induce low affinity IgM
and no memory cells

Front 68

how do you get Hyper IgM immunodeficiency Syndrome in B cell activation?

Back 68

Absence of CD40L/CD40

Front 69

Ag & C3b binding to the BCR of a naïve B-cell (in the absence of a T-cell response) is only capable of producing :

Back 69

IgM
*Class switching to IgG/IgA and affinity maturation that selects for B-cells with higher affinity IgG/IgA will not occur.

Front 70

Plasma cell differentiation and memory B-cells are also not formed without:

Back 70

T-cell interaction

Front 71

This B-cell/T-cell interaction is also important in preventing :

Back 71

Ag production to self-Ag’s, as it is unlikely that both BCR and TCR’s with self-Ag specificity will be present.

Front 72

Ag processing and presentation of Ag by the B-cell (now an APC) through its MHCII molecule to a TCR with Ag specificity will ensure :

Back 72

B-cell class switching, etc.

Front 73

what requires binding of the B-cell CD40 receptor to CD40 ligand (CD40L) on T-cells?

Back 73

Ag processing for B cell activation

Front 74

absence of the CD40L or CD40 is the basis for what disease?

Back 74

the immunodeficient disorder, hyper-IgM syndrome.

Front 75

Th1 cytokines (e.g. IFNg) are very important in regulating :

Back 75

cell-mediated responses to viral infections, graft rejections and tumor immune-surveillance.

Front 76

Poorly controlled Th1 responses are important in :

Back 76

graft rejection, chronic inflammatory disorders, and autoimmune (AI) diseases with primarily a cell-mediated component.

Front 77

Th2 T-cells and cytokines are highly expressed in individuals prone to :

Back 77

allergies (atopic individuals).

Front 78

The type I hypersensitivity response (e.g. anaphylaxis) is dependent on :

Back 78

Th2 polarized (exaggerated) responses.

Front 79

what induces Th17 development?

Back 79

IL-23 induces Th17 development in humans (TGF-b and IL-6 appear to be more important in mice).

Front 80

what Appears to be important in production of cytokines important in granulocyte recruitment and extracellular bacterial/fungal infections.?

Back 80

Th17

Front 81

what appears to play role in chronic inflammatory disease and autoimmune disorders (e.g. Crohn’s, Rheumatoid arthritis, Psoriasis).

Back 81

Th1
Th17

Front 82

is Th17 susceptible to inhibition by Treg cells?

Back 82

barely

Front 83

what's Th17 development blocked by?

Back 83

Th2 cytokine IL-4

Front 84

what does Treg Act to inhibit ?

Back 84

Th1/ Th2

Front 85

what's Very important in preventing AI disease and chronic inflammatory disease?

Back 85

Treg

Front 86

Neoplastic disease often recruits and drives the differentiation of T-cells to the: _________

Back 86

Treg phenotype to prevent the immune system from mounting a response.

Front 87

what are basic differences b/w immature and mature APC?

Back 87

Immature APC:
CD80/86 (B7.1/7.2) Low

Activated APC:
High CD80/86
+ Ag presentation MHCI &II

Front 88

inhibits Th1 and Th2 actions by making TGFbeta and express inhibitory receptors; induce lots of fibrosis- who am I?

Back 88

T reg cell

Front 89

FoxP3 essential for development, won’t turn into Treg cells w/o it; if suppress FoxP3, get _______

Back 89

severe systemic immune disease

Front 90

where do dendritic cells hangout?

Back 90

: hang out in submucosa or subepithelial areas in dermis.. waiting for bac to invade into subepithelial space

Front 91

are dendritic cells professional?

Back 91

very!

Front 92

what happens once immature APC sees bac?

Back 92

gobbles up bac, processes it along w/ MHCI AND II and upregulates CD80/86
also becomes migratory to draining lymph nodes.. hang out in same areas as T cells, presenting antigens to T cells

Front 93

where does APC go for Presentation
of Ag to CD4 & CD8 cells?

Back 93

lymph node

Front 94

what type of APCs inhabit subepithelial spaces?

Back 94

Immature or Naïve professional APCs (dendritic cells)

Front 95

Immature APCs express low levels of ___________

Back 95

CD80/86 (B7.1/7.2) and MHC molecules

Front 96

when are APCs activated?

Back 96

when eat pathogen

Front 97

what's result of APC activation?

Back 97

motile phenotype and migration to draining LNs under control of specific chemokines and chemokine receptors expressed on T-cells and APCs
*up-regulation of CD80/86 and MHC molecules for presentation of Ag to naïve T-cells within the LN

Front 98

how are antigens presented to T cells by APCs in lymph node?

Back 98

often within the high endothelial venules which express adhesion molecules that are expressed by both T-cells and activated APCs (e.g. ICAM-1)).

Front 99

what happens to APC when presentation of Ag in the absence of CD80/86 interaction with the T-cell CD28 receptor ?

Back 99

anergy (inability of the T-cell to respond to Ag challenge)

Front 100

why is anergy of T cell important?

Back 100

key in maintaining peripheral tolerance (e.g. inducing T-cell anergy to self Ag exposure in absence of an inflammatory insult)

Front 101

AI disease is commonly associated with ___________

Back 101

proviral disease

Front 102

a proviral syndrome could induce APC maturation at a time when self-Ags may also being presented to T-cells – resulting in:

Back 102

an inappropriate AI response.

Front 103

what's the purpose of central T cell tolerance?

Back 103

Clonal deletion of self-reactive T cells in thymus.

Front 104

what's 1st step in central T cell tolerance?

Back 104

Positive selection for T-cells recognizing MHC molecules (cells lacking recognition are deleted).

Front 105

what's 2nd step in central T cell tolerance?

Back 105

Second: Negative selection for cells with high affinity interaction with self antigens (cells deleted).

Front 106

Some T-cells that recognize self Ag are converted to ________

Back 106

Treg cells.

Front 107

what Transcriptional regulator induces “peripheral Ag” expression in thymic cells
(Mutated in autoimmune polyendocrinopathy)?

Back 107

AIRE (Autoimmune regulator)

Front 108

: low MHC Class I & II and B7 co-stimulatory molecules is common in what?

Back 108

immature APC cells

Front 109

: Activation by microbial molecules or proteins
released from necrotic cells: Increased MHC & B7 is common in what?

Back 109

mature APC cells

Front 110

what also expresses
inhibitory B7 receptor,
CTLA-4
((-/-) mice assoc. with
AI disease)
Polymorphisms assoc.
with human AI disease?

Back 110

T cells

Front 111

up-regulation of CTLA-4 on T-cells and recruitment of FoxP3+ Tregs is to : ____________ (malicious act)

Back 111

shield the tumor

Front 112

Absent CD80/86 binding during Ag presentation to TCR results in :

Back 112

anergy

Front 113

AI disease is frequently preceded by what?

Back 113

viral infection leading to idea that virally-mediated activation of APCs results in a bystander or coincidental activation of autoreactive T-cells

Front 114

!!

Back 114

Ab’s against CD80/86 have shown promise as co-therapy with tumor vaccines.

Front 115

what is overexpressed on many Treg cells and is also up-regulated in other T-cells following Ag-induced activation?

Back 115

CTLA-4

Front 116

CTLA-4 receptor exhibits much higher affinity for __________, thus inhibiting the actions of _________ leading to loss of ___________

Back 116

CTLA-4 receptor exhibits much higher affinity for CD80/86, thus inhibiting the actions of CD28 leading to loss of T-cell activity or anergy

Front 117

what transcription factor is necessary for Treg differentiation?

Back 117

FoxP3

Front 118

what's the result in animal w/ no Treg gene?

Back 118

AI disease

Front 119

Tregs suppress what? how?

Back 119

Tregs appear to suppress Th1/Th2 responses through at least several mechanisms, including production of anti-inflammatory cytokines (TGF-b/IL-10) and via high expression of CTLA-4.

Front 120

Activated T-cells express high /low levels of Fas ligand (FasL)

Back 120

high!

Front 121

when a previously activated T-cell reencounter Ag presentation to the TCR complex AND the other cell expresses Fas. Fas:FasL interaction in turn results in apoptosis- what is this??

Back 121

activation induced cell death of T cell

Front 122

mutated FAS in humans results in:

Back 122

Autoimmune Lymphoproliferative Syndrome

Front 123

Immune privileged sites (testes, brain, eye, pregnant uterus) utilize high/low levels of Fas, along with high/low expression of MHC molecules (no mature APCs, thus anergy),

Back 123

Immune privileged sites (testes, brain, eye, pregnant uterus) utilize HIGH levels of Fas, along with LOW expression of MHC molecules (no mature APCs, thus anergy),

Front 124

Immature B-cells exposed to high levels of circulating self antigens undergo receptor editing (BCR rearrangements in hypervariable region that do not recognize self).
If not successful, undergo apoptosis
- WHAT'S THIS?

Back 124

central B cell tolerance

Front 125

Requires T-cells. Ag must also be
recognized by Th cells to stimulate B-cell
development.
(Remember CD40:CD40L interaction?)
- WHAT'S THIS?

Back 125

peripheral B cell tolerance

Front 126

*know table on allergy types

Back 126

:)

Front 127

what are the primary mediators of the allergic response?

Back 127

Histamine (Antihistamines):
Chemotactic factors: (LTB4, Eosinophil chemotactic factor)

Front 128

what are secondary mediators (lipid) of allergic response?

Back 128

Cysteinal Leukotrienes (C4, D4), PGD2, PAF
CysLT1 receptor antagonists: zafirlukast (Accolate),
montelukast
(Singulair). 5-LO inhibitors: Zileuton (Zyflow)

Front 129

what are secondary mediators (cytokines) of allergic response?

Back 129

TNF
IL-4, IL-5

Front 130

what's the early response to Type I allergic rxn?

Back 130

Wheel and flare / bronchospasm (LKT C4/D4, PAF) and mucous hypersecretion: vasodilation (histamine, PAF); vascular permeability (histamine, PAF, LKT C4/D4).

Front 131

what's late response to Type I allergic rxn?

Back 131

Recruitment of eosinophils, basophils, neutrophils, CD4+ (TH2). Tissue remodeling

Front 132

what are some bad effects of asthma?

Back 132

Basement membrane thickening
mucus plug
Inflammation with eosinophils
Also: CD4+/Th2 NK-T cells

Front 133

basically, what's a type II hypersensitivity rxn?

Back 133

In all cases:
Immune reaction against
Ab/complement bound to cell or tissue

Front 134

Ab binding to Ag on cell results in complement fixation and opsonization, resulting in lysis or phagocytosis (e.g. transfusion reaction, AI hemolytic anemia, AI thrombocytopenia)
- what's this?

Back 134

Type II: Cytotoxic Antibody Mediated

Front 135

Ab binding to cells activates effector cells: NK cells & also Monocytes, PMNs, Eosinophils, that lyse Ag-coated cells via cytotoxic mechanisms (e.g. granzyme/perforin) (No phagocytosis). Eos use this mechanism to destroy parasites.
- what's this?

Back 135

Type II: Antibody Dependent Cellular Cytotoxicity

Front 136

what's type II hypersensitivity rxn where Antibody has natural
ligand activity?

Back 136

Graves disease

Front 137

what's type II hypersensitivity rxn where Antibody has natural
ligand blocking activity?

Back 137

Myasthenia gravis

Front 138

what Diseases associated with Type II antibody-mediated reactions affects Type IV collagen?

Back 138

goodpasture's syndrome

Front 139

what Diseases associated with Type II antibody-mediated reactions affects skin basement membrane?

Back 139

Bullous pemphigoid

Front 140

what Diseases associated with Type II antibody-mediated reactions affects intrinsic factor?

Back 140

pernicious anemia

Front 141

what Diseases associated with Type II antibody-mediated reactions affects antibodies against streptococcus cross react with heart?

Back 141

Acute rheumatic fever

Front 142

what Diseases associated with Type II antibody-mediated reactions affects Rh D antigen?

Back 142

Erythroblastosis fetalis

Front 143

what Diseases associated with Type II antibody-mediated reactions affects ABO and minor antigens?

Back 143

Transfusion reactions

Front 144

what are Granulomatous lesions that follow necrosis/degenerative phase and precedes fibrosis?

Back 144

Aschoff Bodies:
Hallmark of Rheumatic
Fever

Front 145

For Rheumatic Fever, Ab’s against M-protein of Grp A Strep cross-react with : _________

Back 145

cardiac myofiber protein myosin, heart muscle glycogen and smooth muscle cells of arteries, and perivascular connective tissue

Front 146

The Aschoff body represents an intermediate step that heralds the beginning of the ________

Back 146

repair process for the type II mediated response

Front 147

With Rheumatic Fever, the initial cardiac lesion is one of ________

Back 147

degeneration, with fibrinoid necrosis and acute inflammation

Front 148

The third and final step in Rheumatic Fever is __________--

Back 148

fibrosis (scarring)

Front 149

With continued cross-reacting Ab production, chronic Rheumatic Fever is characterized by _______________

Back 149

repeated acute inflammatory lesions with fibrinoid necrosis, Aschoff body formation and fibrinous resolution

Front 150

The reaction in the tissue is characterized by necrosis, with deposits of “fibrinoid” and an infiltrate of PMNs

Back 150

Type III Prototype: Acute post-streptococcal
glomerulonephritis

Front 151

key diff b/w type II and type III?

Back 151

II: reacts to antigens on cells and tissues
III: reacts to circulating antigens

Front 152

what's disease ex for type II?

Back 152

Goodpasture Syndrome
Anti-Glomerular BM
(collagen IV)
*smooth pattern

Front 153

what's disease ex for type III?

Back 153

Acute post-streptococcal
GN / SLE
*Granular pattern

Front 154

what type is Cell mediated hypersensitivity
No Antibodies?

Back 154

type IV

Front 155

what cytokines are involved in Delayed type hypersensitivity
(Granuloma, tuberculin reaction)
Activated macrophages / histiocytes?

Back 155

CD4+ Th1/Th17

Front 156

what cytokines are involved in Direct cell cytotoxity (graft rejection & virus infection): Perforin/granzyme & FAS/FASL?

Back 156

CD8+ CTL

Front 157

in type IV hypersensitivity, what respond to tissue antigens by secreting cytokines that stimulate inflammation and activate phagocytes, leading to tissue injury. ?

Back 157

CD4+ TH1 cells (and sometimes CD8+ T cells, not shown)

Front 158

in type IV hypersensitivity, what contributes to inflammation by recruiting neutrophils (and, to a lesser extent, monocytes). ?

Back 158

CD4+ TH17 cells

Front 159

what is Reddening and induration peaking at 24-72 hrs.
and
Perivascular infiltration of T cells (CD4+) and mononuclear phagocytes “perivascular cuffing”
?

Back 159

Classic Tuberculin Reaction (PPD)

Front 160

what directly kills tissue cells?

Back 160

CD8+ cytotoxic T lymphocytes (CTLs)

Front 161

what's good and bad about CD8+ cytotoxic T lymphocytes (CTLs) directly kill tissue cells. ?

Back 161

The Good:
Likely important in clearing of virally infected cells / intracellular pathogens & tumor immune surveillance.

The Bad:
Important in mediating graft rejection (Direct Pathway) and some autoimmune diseases

Front 162

Chronic Type IV reactions to persistant or nondegradable Ags (TB and foreign bodies (e.g. sutures) lead to __________ inflammation.

Back 162

granulomatous

Front 163

what's :
Preformed antidonor antibody (ABO incompatibility). RARE
Characterized by Ab: Complement in endothelium
Gross: Pale/cyanotic non-functioning organ
Histology: Rapid thrombotic vasculitis w/ PMN perivascular infiltrates/ischemic necrosis

Back 163

hyperacute rejection

Front 164

can chronic rejection occur with immunosuppressive therapy?

Back 164

YES

Front 165

what are the key pts of the direct pathway of rejection?

Back 165

More prominent in acute rejection
1. Graft APCs present graft Ags to both CD4 (MHCII) & CD8 (MHCI).
2. Type IV CD8+ cytoxic T-cell mediated cell killing is prominent. Cause of tubular damage in acute & chronic rejection.
3. CD4+ response exhibits greater Th1-mediated activation of monocytic phagocytes.

Front 166

what are the key pts of the indirect pathway of rejection?

Back 166

More prominent in chronic rejection
1. Recipient APCs present graft Ags (MHCI recognized as self-thus CD8+ response suppressed) Thus, indirect rejection requires MHCII- mediated activation of CD4+ cells only.
2. Limited to CD4+ cell delayed type hypersensitivity responses mediated by cytokines

Front 167

in either direct or indirect pathway, Ab mediated rejection is mediated by?

Back 167

rejection vasculitis (treat with B-cell depleting therapies), cell-mediated rejection is characterized by tubular interstitial inflammatory cells (lymphocytes and mononuclear cells).

Front 168

what's this? Can range from Necrotizing vasculitis (more acute-Ab mediated activation of phagocytes) to less acute: Intimal thickening with inflammatory cells, foamy macrophages and smooth muscle proliferation
Need B-cell depleting therapy:

Back 168

Acute Humoral Rejection: Type II Antibody Mediated

Front 169

what's this:
Transplanted T-cells recognize
recipient as “foreign” and mount
rejection response.
Treatment with High dose steroids
and anti-thymocyte globulins
High mortality rate: sepsis
T-cell Depletion (anti-T cell antibodies)?

Back 169

Graft vs. Host Disease
Bone Marrow Transplants