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IMMUNOLOGY > IMMUNOLOGY QUIZ 2 > Flashcards

IMMUNOLOGY QUIZ 2 Flashcards

0
Q

TYPE I HYPERSENSITIVITY CELLS and ANTIBODIES

A

mast cells and basophils with preformed histamine and high affinity receptors for IgE.
IgE

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1
Q

CD40 LIGAND/CD154

A

made by CD4+ Th2 cells to stimulate B cells isotype switching. Binds to CD40 on B cell surface.

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2
Q

TYPE II HYPERSENSITIVITY CELLS AND ANTIBODIES

A

CELLS: macrophages, NK cells, neutrophils, eosinophils
Antibodies: IgG, IgM, complement

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3
Q

TYPE III HYPERSENSITIVITY CELLS AND ANTIBODIES

A

Ag-Ab complexes (mostly IgM and IgG), complement

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4
Q

TYPE IV HYPERSENSITIVITY CELLS AND ANTIBODIES

A

CELLS: sensitized T cells, NK cells, macrophages

no antibodies

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5
Q

TYPE I HYPERSENSITIVITY TIME COURSE AND CLINICAL CONSEQUENCES

A

Timing: Occur after prior sensitization. Occurs within minutes.
Consequences:
skin: edema, wheal, flare, hives
pulmonary: bronchospasm, edema
CV: hypotension, arrhythmias, CV collapse
GI: cramps, vomiting, diarrhea

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6
Q

How does histamine mediate IMMEDIATE hypersensitivity?

A

Histamine: act on H1 receptors (contract SM, increase mucous, increase vascular permeability), act on H2 receptors (increase gastric secretion, decrease mediator released by basophils and mast cells).

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7
Q

How does PROSTAGLANDIN mediate IMMEDIATE hypersensitivity?

A

vasodilation, edema, bronchoconstriction.

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8
Q

How do SRS-A and Leukotrienes C4, D4, E4 mediate IMMEDIATE hypersensitivity?

A

constrict airways, increased permeability of vessels, vasodilation, increase mucous.

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9
Q

How does LEUKOTRIENE B4 mediate IMMEDIATE hypersensitivity?

A

causes neutrophil chemotaxis, adhesion of neutrophils to endothelium, neutrophil degranulation.

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10
Q

How do PAF mediate IMMEDIATE hypersensitivity?

A

produced by mast cells. Aggregate platelet, vasodilation, bronchoconstrictor, chemotaxis and degranulation in eosinophils and neutrophils.

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11
Q

How do PROTEASES mediate IMMEDIATE hypersensitivity?

A

activate kinins, complement, vascular permeability?

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12
Q

What are the mediators of PRO-INFLAMMATORY reactions by chemotaxis and mast cell activation?

A
  1. Leukotriene B4
  2. IL-8, C5a, PAF
  3. Anaphylatoxins (C3a, C4a, C5a)
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13
Q

What are the TREATMENTS for Type I hypersensitivity?

A
  1. Histamine receptor antagonists (benadryl)
  2. Leukotriene receptor antagonists
  3. IgE antibodies
  4. Synthetic glucocorticoids
  5. Epinephrine and long acting beta-2 receptor agonists
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14
Q

What is SCIT?

A

Treatment of TYPE I hypersensitivity. Involves hyposensitization subcutaneously. Activate T-reg cells to increase allergen-specific IgG and IgA that decrease allergic reactions (divert attention away from IgE).

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15
Q

What are genetic and environmental factors that influence allergies?

A
  1. HLA - associate with particular antigens

2. Environment: living on farms (decrease risks of asthma), exposed to things are good.

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16
Q

Mast cell

A

Have granules preloaded with Histamines and other enzymes.
Have high affinity FcERI (receptors for IgE Fc region).
IgE + Ag activate mast cells to degranulate WITHIN SECONDS.

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17
Q

Basophils

A

Also release mediators with mast cells.
Also have FcERI.
Have H2 receptors that provide NEGATIVE FEEDBACK to subdue mediator release.

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18
Q

Sensitization

A

After first exposure to allergen –> activates Th2 cells –> stimulate class switching of IgE in B cells –> produce IgE –> binding of IgE to FcERI on mast cells.

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19
Q

IgE

A

VERY short half-life.
very high affinity for mast cells
TISSUE half-life is LONG.

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20
Q

Fc-gamma Receptor

A

Receptors for IgG Fc region. Has LOW AFFINITY and INHIBITS B cell, mast cell, and DC activation.

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21
Q

Hyposensitization

A

Downregulate Th2.
Upregulate Th1.
Involves SCIT by incrase doses of antigen to activate T-REGS and increase IgG and IgA.

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22
Q

Atopy

A

Presence of specific IgE antibodies against common environmental allergens.

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23
Q

ADCC

A

Antibody dependent cellular cytotoxicity. Antibody coats cell –> trigger Fc-gamma RIII binding by NK, PMN cells –> release toxic molecules –> lysis of antibody-coated cell.

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24
Q

C3a and C5a

A

anaphylotoxins that also activate mast cells, neutrophil. Bind to C’ receptors on mast cells and endothelial cells that lead to edema and leakage.
C5a is a chemotactant for neutrophils.

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25
Q

Immune complex

A

formed by circulating antigens + IgM/IgG antibodies that are deposited in vascular basement membrane.

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26
Q

Hyperacute rejection

A

Example of Type II hypersensitivity.
Occurs quickly within HOURS.
Mediated by preformed allo-antibodies.
Leads to: complement activation, endothelial damage, inflammation, thrombosis.

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27
Q

Hapten

A

from drugs or drug metabolites that associate with host cell membrane proteins.
Cannot induce immune response by itself.
Needs to be in a hapten-carrier complex that can activate complement and Fc receptor-dependent clearance.

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28
Q

HDN (erythroblastosis fetalis)

A

Mother who is Rh-D NEGATIVE has first child that is Rh-D POSITIVE.
Mother and first child will be fine.
Mother will form anti-D antibodies.
Second child that is Rh-D POSITIVIE is at risk for being exposed to mother’s anti-D antibodies. Will be killed if exposed.

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29
Q

Treatment for HDN

A

Give mothers who are Rh-D NEGATIVE –> RHESUS PROPHYLAXIS that have anti-RhD antibodies.

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30
Q

C’ (complement receptors)

A

Present on mast cells and endothelial cells.

Bind to C3a and C5a leading to blood vessel leakage and edema.

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31
Q

Isohemagglutinins

A

Alloantibodies that are naturally a part of ABO system. Antibodies to A and B antigens. First detected within 3-6 months of age.

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32
Q

Serum sickness

A

Classical example of IMMUNE COMPLEX DISEASE (Type III hypersensitivity).
Common in pre-antibiotic era when serum is used to passively immunize people.

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33
Q

Immune thrombocytopenic purpura

A

Autoimmune disease.
IgG antibodies are made against platelets by both the Fab and Fc domains. After flu infection, platelets can bind to immune complexes at Fc domains and lead to THROMBOCYTOPENIA.

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34
Q

ABO incompatibility

A

Type II hypersensitivity.
ABO antigenic differences are due to specific terminal sugar residues. Lead to enabling of alloantibodies that recognize foreign antigen.
Mismatch = immedate agglutination, complement-mediated lysis, phagocytosis by macrophages in liver or spleen.

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35
Q

TRALI

A

Type II hypersensitivity
Transfusion related to acute lung injury.
Antibodies in donated plasma will bind to recipient’s cells and induce serious reactions.

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36
Q

Hyperacute graft rejection

A

Type II hypersensitivity.
Occurs very quikcly.
Transplant recipient already been sensitized to antigens on graft tissues.
Have preformed alloantibodies.
ONLY occurs when grafts are REVASCULARIZED DIRECTLY during transplantation.
Can lead to complement activation.

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37
Q

Contrast serum sickness and Arthus reaction

A

Similar: soluble Ag injected intradermally that combines with excess Ab to form immune complexes and precipitates in venules. Causes local erythema and edema.
Difference: Arthus is local. Serum is systemic.

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38
Q

C3b and Type III hypersensitivity

A

C3b is deposited on immune complex –> binds to CR1 receptors on erythrocytes –> sequesters the complex and bring to liver and spleen for elimination.

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39
Q

TYPE IV Hypersensitivity Onset and Duration

A

Onset: 15 hours
Duration: 5 days

40
Q

Type I Hypersensitivity Onset and Duration

A

Onset: minutes
duration: 1 hour

41
Q

Type III hypersensitivity onset and duration

A

onset: 2 hr
duration: 24 hr

42
Q

Does DTH/TYPE IV Hypersensitivity depend on serum or antibodies?

A

NO!

43
Q

Type IV Hypersensitivity key cytokines

A

IFN-gamma and TNF-alpha released by Th1

44
Q

Contact - TYPE IV Hypersensitivity

A

Reaction time: 48-72 hr
Clinical appearance: eczema
histology: lymphocytes, later macrophages, edema of epidermis
antigen: Nickel, rubber, poison ivy
Involves: haptens, interact with skin DCs, cytotoxic T cells

45
Q

Tuberculin - Type IV Hypersensitivity

A 
Reaction time: 48-72 hr
Clinical appearance: local induration
Histology: lymphocytes, macrophages, monocytes
Antigen: intradermal tuberculin
Involves: IFN-gamma, TNF-alpha, Th1
46
Q

Granuloma - Type IV hypersensitivity

A

Reaction time: 21-28 DAYS
Clinical appearance: hardening (skin or lung)
Histology: macrophages, epithelial cells, giant cells, fibrosis
Antigen: persistent Ag or Ag/Ab complexes, non-immunoglobulin stimuli
Involves: PERSISTENT antigens, formation of granulomas by activated T cells to wall off bacteria.

47
Q

Autoimmune hemolytic anemia (AIHA)

A 
Autoimmune disease (duh).
Affects RBCs.
IgG autoantibodies bind to RBCs --> trigger complement and/or Fc receptor-mediated clearance --> destroy RBCs.
48
Q

Myasthenia Gravis (MG)

A

Autoimmune disease.
Affect muscles –> weakening and tired.
Antibodies against Ach receptors –> BLOCKS Ach binding sites –>trigger complement or non-complement activation –> can crosslink receptors –> receptors become internalized or non-functional.

49
Q

Grave’s Disease

A

Autoimmune disease.
Affect thyroid.
TSHR-specific autoantibodies ACTIVATE TSH receptor –> increase thyroid hormone synthesis. Also greater uptake of iodide.

50
Q

Hashimoto’s Thyroiditis

A

Autoimmune disease.
Opposite of Grave’s.
Autoantibodies INHIBIT thyroid function rather than stimulating it.

51
Q

Systemic Lupus Erythematous (SLE)

A

Autoimmune disease.
Affect vasculature and kidneys. Could also be systemic.
Formation of toxic immune complexes that damage organs via COMPLEMENT activation.
Due to persistent autoantibody from LACK of downregulation by T-regs or CD8+ suppressor T cells.

52
Q

Central Tolerance

A

Location: thymus and bone marrow.
When immature lymphocytes recognize self-antigens.
Lead to:
1. apoptosis
2. receptor editing
3. differentiate into suppressive T-regs (true for CD4 T cells only)

53
Q

Peripheral tolerance

A 
Location: peripheral tissues
When MATURE lymphocytes that can recognize self.
Lead to:
1. anergy (with no costimulation)
2. apoptosis
3. suppressed by T-regs
54
Q

Cross-reactive epitopes and autoimmunity

A

Active response against a COMMON epitope seen in BOTH microbe and host tissue. Host tissue may be attacked.

55
Q

Sequestered autoantigens theory

A

During embryonic development.
Antigens that are ABSENT or SEQUESTERED will NOT be recognized as self and not be “tolerated.”
Later exposure in life from infection or trauma can lead to autoimmune disease.

56
Q

Are men more likely to have autoimmunity?

A

NO!

More likely in women. Evidence: mice with ovaries removed and treat with testosterone gets SLE-like disease.

57
Q

Treatments for autoimmune diseases

A
  1. NSAIDs, glucocorticoids
  2. Lymphoid irradiation –> eliminate bone marrow derived immune cells
  3. Rituximab –> deplete B cells
  4. Plasmapheresis –> removal and replacement of plasma. Short-lived efficacy.
  5. IVIG: modulate function of Fc receptors, interfere with complement activation.
58
Q

Adjuvant

A

enhances body’s immune response to an antigen. Infections can lead to adjuvant effect that UPREGULATES expression of receptors (TLRs) and cytokines.
Can be bad when it facilitates responses against weak SELF-ANTIGENS.

59
Q

Idiotope

A

Epitopes unique to an antibody’s variable region.

60
Q

Autograft

A

Graft to self. Can take core blood for bone marrow transplant.

61
Q

Syngeneic graft

A

Grafting between IDENTICAL twins.

62
Q

Allograft

A

Graft between NON-IDENTICAL individuals. Can work but need immune suppression. Need to match HLA.

63
Q

Xenograft

A

Never work. Immune system reject.

64
Q

Immunologic laws of transplantation

A
  1. graft rejection is CELL mediated. B-cell deficient animals can still reject grafts.
  2. graft rejection shows MEMORY. Rejection against second graft is MORE RAPID and EFFECTIVE.
  3. graft rejection shows SPECIFICITY. Rejection is accelerated from second allograft of same individual, but not from 3rd individual.
65
Q

Major antigens in graft rejection

A

MHC I AND II

You want to match MHC II first - mismatching MHC II will significantly decrease survival.

66
Q

Minor antigens in graft rejection

A

polymorphisms between individuals. Major reason for difficulty in matching.

67
Q

Ways that T cells recognize grafts as foreign

A
  1. Direct allorecognition: major pathway. T cell recognizes unprocessed allogeneic MHC molecule on GRAFT APCs.
  2. Indirect allorecognition: minor pathway. T cell recognizes processed peptide of allogeneic MHC bound to self MHC molecule on host APC.
68
Q

3 Types of allograft rejection

A
  1. Hyperacute: within hours. Based on PREFORMED antibodies. Antibodies bind to alloantigen and lead to complement activation.
  2. Acute: within days. Based on ALLOREACTIVE CD8+ T cells and alloreactive antibodies. Should NOT happen if HLA is matched and by immunosuppression.
  3. Chronic: in months - years. By macrophages. Hard to control.
69
Q

Bone marrow transplantation

A

match needs to be MUCH closer because of Graft vs. Host disease. Graft can recognize HOST as foreign.

70
Q

3 Stages of Immune Editing

A

Tumor immunology.

  1. Elimination: NK cells and T cells infiltrate tumors and eliminate or fail to eliminate.
  2. Equilibrium: tumors remain dormant for years due to constant pressure of CD8 T cells and NK cells.
  3. Escape: tumor mutates and can evade host immune response and grow to clinically evident disease.
71
Q

TSAs

A

Tumor Specific Antigens = unique to tumor cells

72
Q

TAAs

A

Tumor Associated Antigens = can ALSO be found on normal cells.

73
Q

Viral antigens

A

A type of tumor antigen.
Strongly antigenic.
Ex: HPV, Hep B and C, EBV, HTLV.
Cancers arise in immunosuppressed individuals.

74
Q

Oncofetal antigens

A

Tumor antigen.
Also found on embryonic or fetal cells.
Considered TAA’s.
Ex: CEA and AFP.

75
Q

Why are mutated antigens good targets for T cells?

A

Mutated proteins are DIFFERENT from normal protein counterparts. T cells can recognize these antigens (no central or peripheral tolerance).

76
Q

How are mAbs used for immunodiagnosis?

A

mAbs to oncofetal antigens can be used for diagnosis. Anti-CEA can monitor CEA concentration in serum (indicates tumor burden). Can also be used for IHC analysis of who tissues or body imaging.

77
Q

How can differentiation antigens provide information on tumor cell lineage?

A

many tumors arise from a single cell ARRESTED at some point in differentiation. We can use mAb to differentiation antigens to determine approximate stage of differentiation that malignancy has occurred. Useful for leukemias and lymphomas.

78
Q

What is the connection between tumor immunity and autoimmunity?

A

If the differentiation antigens on tumors are also expressed by normal cells. Ex: melanoma antigens that are also expressed on normal melanocytes.

79
Q

How does Adoptive T cell Therapy work?

A

T cells engineered to express TCRs specific for tumor antigens. Gets re-infused in patients. Patients need to undergo irradiation first to make room for the new T cells.

80
Q

Primary immunodeficiency

A

Congenital. Failure of proper development of humoral or cellular immune systems. Rare.

81
Q

Secondary immunodeficiency

A

Acquired. Consequences of other diseases and their treatments.

82
Q

B cells immunodeficient

A

Lead to bacterial infections

83
Q

T and B combined immunodeficient

A

viral, fungal, bacterial, protozoal infections

84
Q

T cells immunodeficient

A

viral, fungal, protozoal infections

85
Q

phagocyte immunodeficient

A

bacterial infections

86
Q

complement immunodeficient

A

bacterial infections, autoimmunity

87
Q

SCID

A

Severe combined immunodeficiency. Affects both T and B cells development.

88
Q

X-linked SCID

A

Affect cytokine gamma chain. Pro-T cells cannot differentiate into immature T cells.

89
Q

Bruton’s Disease

A

XLA defective gene –> defective btk –> B cells do not mature. Normal T cells

90
Q

Hyper-IgM syndrome

A

B cells do NOT switch class from IgM. No IgG. Defective gene encoding CD40 on B cells or CD40L on T cells.

91
Q

Di George Syndrome

A

Lack of a thymus –> defect thymus embryogenesis. T cells will NOT mature.

92
Q

CGD (Chronic Granulomatous disease)

A

defect in genes for NADPH oxidase –> defective intracellular killing of bacteria. Mostly X-linked. Viral infection responses are normal.

93
Q

LAD (Leukocyte adhesion deficiency)

A

Absence of leukocyte adhesion molecules.

94
Q

C1, C2, C4 deficiencies

A

Immune complex disease –> cannot remove immune complexes.

Resembles: SLE (kidney issues, vasculitis).

95
Q

C3, factors H&I deficiencies

A

very serious. Repeated infections.

96
Q

C5-C9 deficiencies

A

no MAC –> repeated infections with Neisseria bacteria.

97
Q

C1q inhibitor deficiency

A

Lead to hereditary angioedema because of CONTINUOUS complement activation and consumption.

IMMUNOLOGY (1 decks)

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