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FMS Week 9 > Week 9 review > Flashcards

Week 9 review Flashcards

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1
Q

Central T cell tolerance

A

Negative selection of high affinity T cells in the thymus

expression of tissue specific proteins in the thymus (via AIRE) so that they participate in negative selection of T cells

positive selection in the thymus serts an affinity threshold

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2
Q

Peripheral tolerance of T cells

A

suppression of responses by regulatory T cells (which compete for growth factors, secrete inhibitory cytokines, and directly inhibit T cells)

unresponsiveness of T cells without co-stimulatory signals

exclusion of lymhocytes from certain peripheral tissues (brain, eyes, testes)

Downregulation of responses (CTLA-4, PD-1, Fas/FasL killing)

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3
Q

No autoreactive TH cells means…

A

no autoantibodies

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4
Q

If B cell sees self antigen but it does not get T help,

A

it will not get activated

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5
Q
A

Overview of B cell tolderance

negative selection in the bone marrow

if B cell sees self antigen but doesnt get T help it will not be activated

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6
Q

Which of the following is a PERIPHERAL tolderance mechanism used by both B and T cells?

Negative selection

regulatory T cells

receptor editing

antigen sequestration

allelic exclusion

A

ANTIGEN SEQUESTRAITON

negative selection-central tolerance mechanism

regulatory T cells- can down regulate T helper

receptor editing- B cells in the bone marrow. CENTRAL.

allelic exclusion- doesnt mean anything

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7
Q

Which one of the following statements concearning autoimmune disease is true?

autoimmunity manifests as organ-specific, not systemic, disease

infectious organisms are frequently present in autoimmine lesions

effector mechanisms in autoimmunity include curculating autoantibodies, immune complexes, and autoreactive T lymphocytes

among the genes associated with autoimmunity, associations are particularly prevalent with class I MHC genes

many autoimmune diseqases show higher incidence in males than females

A

effector mechanisms in autoimmunity include curculating autoantibodies, immune complexes, and autoreactive T lymphocytes

autoimmunity is more associated with class II MHC genes

autoimmunity usually higher in males than females

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8
Q

Type I hypersensativity

A

AKA immediate hypersensativity

TH2 cells, IgE, mast cells, eosinophils

mechanism of injury
mast cell derived mediators (vasoactive amines, lipid mediators, cytokines)

cytokine mediated inflammation (eosinophils, neutrophils)

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9
Q

Type II hypersensativity

A

antibody mediated

IgM, IgG antibodies against cell surface or ECM antigens

Complement and Fc receptor mediated recruitment and activation of leukocytes (neutrophils, macrophages)

opsonization and phagocytosis of cells

abnormalities in cellular function ed hormone receptor signaling

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10
Q

Type III hypersensativity

A

immune complex mediated

Immune complexes of circulating antigens and IgM or IgG antibodies deposited in basement membrane

complement and Fc receptor mediated recruitment and activation of leukocytes

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11
Q

type IV hypersensativity

A

T cell mediated diseases

CD4+ T cells, (delayed type hypersensativity)

CD8+ CTLs (T cell mediated cytolysis)

macrophage activation, cytokine mediated inflammation

direct target cell lysis, cytokine mediated inflammation

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12
Q

DTH and PPD antigens

A

type IV hypersensativity

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13
Q

Autoimmune hemolytic anemia

A

Type II hypersensativity

Target antigen: erythrocyte membrane protein

mechanism of disease: opsonization and phagocytosis of RBC

clinicopathologic manifestations: hemolysis, anemia

LYSIS OF CELL

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14
Q

Autoimmune (idiopathic) thrombocytopnic purpura

A

Type II hypersensativity

Target antigen: PLATELET MEMBRANE

mechanism of disease: OPSONIZATION AND PHAGOCYTOSIS OF PLATELETS

clinicopathologic manifestations: BLEEDING

lysis of cells!

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15
Q

Pemphigus vulgaris

A

Type II hypersensativity

Target antigen: proteins in intracellular junctions of epidemal cells (epidermal cadherins)

mechanism of disease: antibody mediated activation of proteases, disruption of intracellular adhesions

clinicopathologic manifestations: skin vessicles (bullae)

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16
Q

Goodpastures syndrome

A

Type II hypersensativity

Target antigen: noncollagenous protein in basement membranes od kidney glomeruli and lung alveoli

mechanism of disease: complement and Fc receptor mediated inflammation

clinicopathologic manifestations: nephritis, lung hemorrhages

inflammation

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17
Q

Acute rheumatic fever

A

Type II hypersensativity

Target antigen: streptococcal cell wall antigen; antibody cross-reacts with myocardial antigen

mechanism of disease: inflammation, macrophage activation

clinicopathologic manifestations : myocarditis, arthritis

MOLECULAR MIMICRY

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18
Q

Myesthenia gravis

A

Type II hypersensativity

Target antigen: Ach receptor

mechanism of disease: antibody inhibits acetylcholine binding. Down modulates receptors (ab blocks binding site)

clinicopathologic manifestations: muscle weakness, paralysis

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19
Q

Graves disease (hyperthyroidism)

A

Type II hypersensativity

Target antigen: thyroid stimulating hormone receptor (TSH)

mechanism of disease: antibody mediated stimulation of TSH receptors

clinicopathologic manifestations: hyperthyroidism

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20
Q

Pernicious anemia

A

Type II hypersensativity

Target antigen: intrinsic factor of gastric parietal cells

mechanism of disease: neutralization of intrinsic factor. decreased absorption of vitamin B12

clinicopathologic manifestations: abnormal erythopoesis, anemia

AB MEDIATED INHIBITION OF FUNCTION

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21
Q

Systemic lupus erythematosus

A

Type III hypersensativity

Antibody specificity: DNA, nucleoproteins, others

Clinical manifestations: nephritis, arthritis, vasculitis, renal failure

Antibuclear Abs (ANA)

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22
Q

Serum sickness (clinical and experimental)

A

Antibody specificity: various protein antigens

Clinical manifestations: systemic vasculitis, nephritis, arthritis

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23
Q

SLE

A

displays more than one type of hypersensativity reaction

immune complexes (type III) mediating vasculitis, serositis,glomerulonephritis, arthritis, rash and oral ulcers, pericardial and pleural effusions,

Coomb’s positive hemolytic anemia (type II)

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24
Q

Type 1 (ID) DM

A

Type IV hypersensativity reaction

Specificity of pathogenic T cells: pancreatic islet antigens

Genetic associations: insulin, PTPN22

Clinicopathologic manifestations: impaired glucose metabolism, vascular disease

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25
Rheumatoid arthritis
Type IV hypersensativity reaction Specificity of pathogenic T cells: unknown antigens in joint Genetic associations: PTPN22 Clinicopathologic manifestations: inflammation of synovium and erosion of cartilage and bone in joints
26
multiple sclerosis
Type IV hypersensativity reaction Specificity of pathogenic T cells: myelin proteins Genetic associations: CD25 Clinicopathologic manifestations: demyelination of neurons in the CNS, sensory and motor dysfunction
27
Contact sensativity (eg poison ivy reaction)
Type IV hypersensativity reaction Specificity of pathogenic T cells: modified skin proteins Clinicopathologic manifestations: DTH reaction in the skin, rash
28
Superantigen mediated diseases (toxic shock syndrome)
Type IV hypersensativity reaction Specificity of pathogenic T cells: polyclonal (microbial superantigens activate many T cells of different specificites Clinicopathologic manifestations: fever, shock related to systemic inflammatory cytokine release Superantigen mediated- pathogen (microbial superantigen) activated T cells
29
Hypersensativity and allergy
Components: TH2, IgE, mast cells (mucosal/connective tissue), basophils (blood), and eosinophils (blood) Mechanism of injury: mast cell derived mediators such as vasoactive amines such as histamine, lipid mediators, and cytokines ( IL4, IL5, IL13) Processes: vascular dilation (vasoactive amines and prostaglandins) Tissue damage (proteases) Smooth muscle contraction ( vasoactive amines and leukotrienes) inflammation and recruitment of leukocytes (cytokines)
30
Steps in allergy
first exposure to allergen antigen activation of TH2 cells and stimulation of IgE class switching in B cells Production of IgE Binding of IgE to FCeRI on mast cells Repeate exposure to allergen activation of mast cells and release of mediators Vasoactive amines, lipid mediators: immediate hypersensativity reaction (minutes after repeat exposure to allergen) Cytokines: late phase reaction (6-24 hours after repeat exposure to allergen)
31
In an experiment, antigen is used to induce immediate (type I) hypersensativity response. Cytokines are secreated that are observed to stimulate IgE production by B cells, promote mast cell growth, and recruit and activate eosinophils in this response. Which of the following cells is the most likely to be the source of these cytokines? TH2 cells TH1 cells Mast cells Eosinophils Dendritic cells
TH2 cells
32
A woman who is allergic to cats visits a neighbor who has several cats. During the visit she inhales cat dander, and within minutes, she develops nasal congestion and abundant nasal secretions. Which of the following substances is most likely to produce these findings? Complement C5a Histamine IL-1 Phospholipase C Numor Necrosis Factor (TNF)
HISTAMINE
33
Mediators stored in preformed cytoplasmic granules
Immediate response histamine enxymes: tryptase, chymase, carboxypeptidase, cathepsun G TNFalpha
34
Histamine
increases vasc perm, stim smooth muscle cell contraction, toxic to parasites
35
Enzymes: tryptase, chymase, carboxypeptisase, cathepsin G
tissue damage/ remodeling; degrades microbial structures
36
TNF alpha
promotes inflammation, activated endothelium immediate response
37
Major lipid mediators produces on activation
late phase response prostaglandin D2 Leukotriene C4, D4, E4 Platelet activating factor
38
Prostaglandin D2
vasodilation, bronchoconstriction, neutrophil chemotaxis
39
Leukotriene C4, D4, E4
prolonged bronchoconstriction mucus secretion increased vasc perm
40
platelet activating factor
late phase response lipid mediator chemotaxis and activation of leukocytes (eosinophils and neutrophils) and platelets, bronchoconstriction, increased vasc perm
41
Cytokines/ chemokines produced on activation (by mast cells after cross linking)
IL3 TNF alpha IL4 IL13 IL5 CCL3
42
IL3
promotes mast cell proliferation
43
TNFa
promotes inflammation
44
IL4 IL13
promotes Th2 differentiation, mucus production
45
IL5
promotes eosinophil production and activation
46
CCL3
chemotactic for monocytes, macrophages, neutrophils
47
Type I hypersensativity reaction of skin
wheal and flare (immediate) Swelling (late phase)
48
Type I hypersensativity reaction of resp tract
rhinitis polyps asthma eosinophils
49
Type I hypersensativity reaction of digestive tract
diarrhea, cramps, vomiting
50
Type I hypersensativity reaction systemimc
anaphylactic shock edema circulatory collapse tracheal occlusion
51
Hyperacute rejection
minutes to hours rapid and mediated by circulating antibodies which activate coplement, leading to endothelial damage and thrombosis Already circulating Abs against something in graft
52
Accelerated rejection
days reactivation of sensitized T cells
53
Acute rejection
days to weeks mediated by T. cells which react against the alloantigens in the graft direct allorecognition
54
chronic rejection
months to years mediated by T helper cells, which secrete cytokines which stimulate cellular proliferation indirect allorecognition
55
Graft vs host disease
follows bone marrow transplantation. Transplanted mature T. cells recognise self tissue as foreign
56
Hyperacute rejection
preexisting Abs against ABO, HLA, other bind to transplant tissue, then induce inflammation
57
Acute rejection
direct allorecognition of donor MHC by recipient T cell (can lead to killing by alloreactive CD8 cells and or the induction of anti graft antibodies upon CD4 T cell activation
58
Chronic rejection
often indirect allorecognition in which in the MHC fron the donor is presented to recipient T cells, initiating B and T cell responses against the donor tissue
59
Graft vs host disease occurs when
The graft contains mature T cells (newly emerging T cells will be educated in the recipients thymus) There must be some histoincompatibility (MHC or minor histcompatability antigens) The recipient must be immunocompromised ( otherwide the transplanted cells will be destoryed)
60
How could an MHC mistmatch upon HSC transplant affect T cell responses
You get a bone marrow transplantation and then the donor HSC reconstitutes recipients HSC system (T cells and APCs come from donor) Positive selection in the thymus. Donor T cell sees recipient thymic epithelial cells Recipient and donor not HLA matched upon infection, donor APC in periphery present pathogen derived peptides to donor T cells No adaptive immune response. Infection persists
61
The patient had pre-formed antibodies specific for alloantigens on graft endothelial cells
62
Immunosuppressive drugs, such as cyclosporine, are effective in preventing or treating this type of rejection acute rejection mediated by T cells specidic for alloantigens in the heart. Chronic is not likely at 14 weeks
63
CD8+ lymphocytes
64
Activation of tumor specific T cells specific for tumor antigens (usually tumor associated neoantigens) and the adjuvsants taht can promote and anti-tumor response
Problem: Tregs tumor evolution
65
Isolation, expansion, and re-infusion of tumor infiltrating lympho cytes
problem logistics
66
Blocking immunosuppressive mechanisms that inhibit anti-tumor responses ( such as CTLA-4, PD-1, and regulatory T cells)
problem: autoimmunity
67
genetically modifying T cells so that they targer tumors (CAR-T cells)
Problem cytokine storm
68
The use of monoclonal antibodies against tumor antigens
problem anti-mab abtibodies tumor evolution
69
Autoimmunity
blocking T cell activation using soluable CTLA-4 involved in down regulating immune responses (T cell)
70
Cancer immunotherapy
preventing T cell inhibition by blocking CTLA-4 or PD-1 using monoclonal antibodies
71
What are chimeric antigen receptors?
making artificial receptor that binds to a tumor antigen signaling domain is similar to a T cell receptor. Activated in the same way T cell is. Will kill Advantages: many more cells specific for tumors much higher affinity for tumor cells
72
Which of the following statements about immune response to tumor is true? T. cells specific for tumor antigens. cannot be found in most human tumor patients Antibodies specific for tumor antigens cannot be found in many human tumor patients The presence of lymphocytic infiltrates in certain tumors is associated with a worse prognosis than lymphocyte poor tumors of the same histologic type immunodeficient individuals are more likely to develop certain cormas of cancer than are immunocompetent individuals the host immune response us usually capable of eradicating common tumors once they are established
immunodeficient individuals are more likely to develop certain cormas of cancer than are immunocompetent individuals ## Footnote infiltrating T lymphocytes good
73
To stimulate CD8+ T lymphocytes targeting cells that express E6 and E7 E6 and E7 expressed in cytosol. Abs probably wouldnt work.
74
It prevents costimulation of T cells by antigen presenting cells
75
Inhibition of B cell activation by Th cells

FMS Week 9 (2 decks)

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