Immuno

Front 1

Autograft

Back 1

a graft transplanted into the same individual from which it came

Front 2

Syngeneic Graft

Back 2

a graft transplanted between genetically identical individuals

Front 3

Circumstances conducive to formation of immune complexes (3)

Back 3

1. Persistent low grade infection
2. Autoimmunity (antigens always present)
3. Formation at body surfaces

Front 4

Farmer's Lung Disease

Back 4

Circulating antibodies trigger inflammation and compromise lung function
From repeated exposure to moldy hay

Front 5

How are immune complexes usually destroyed? (2) Where?

Back 5

Phagocytosis in the liver/spleen
RBC's bind compliment that has been fixed by the complexes, then removed by hepatic macrophages

Front 6

What happens after complexes deposit in tissues?

Back 6

1. They activate compliment
2. Compliment activation leads to recruitment and activation of inflammatory cells
3. Neutrophils cause tissue injury

Front 7

What size complexes are most prone to deposition in tissues?

Back 7

Intermediate

Front 8

What factors influence the deposition of immune complexes?

Back 8

1. Size - intermediate deposit more readily
2. Clearance rate
3. Charge - + charged complexes bind to - charged components of the glomerular basement membrane
4. Anatomic factors - filtering and tortuous vessels

Front 9

What causes chronic serum sickness?

Back 9

Multiple injections of antigen or continual exposure to self antigens

Front 10

What does chronic serum sickness cause?

Back 10

Formation of smaller complexes that deposit in kidneys, arteries, lung vasculature

Front 11

Systemic Lupus Erythematosus

Back 11

small complexes deposited in the blood

antibodies are produced against nuclear antigens such as DNA

Front 12

Arthus Reaction

Back 12

antigen injected subcutaneously

individual already has antibodies for that antigen
complexes form and deposit in the walls of the small arteries at the injection site.
= local cutaneous vasculitis with necrosis

Front 13

Hypersensitivity reactions of the eye
(2)

Back 13

1. Peripheral corneal lesions
2. Uveitis

Front 14

How long does type 4 hypersensitivity reaction take to develop?

Back 14

More than 12 hours

Front 15

Two types of delayed type hypersensitivity

Back 15

1. Contact hypersensitivity
2. Tuberculin-type hypersensitivity

Front 16

What causes blistering in contact hypersensitivity?

Back 16

T cells and macrophages gather around the local vasculature int he dermis.
These cells infiltrate into the epidermis, where they act to eliminate the antigen.

Front 17

What is the hallmark of a TB-type hypersensitivity?

Back 17

Induration (hardness)

Front 18

What causes the hardness in TB-type hypersensitivity?

Back 18

T cells and macrophages gather in the dermis

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Langerhan's Cells

Back 19

specialized APC's in the epidermis that process antigens then migrate to the draining lymphnodes where they present their antigen to the T cells, activating them.

Front 20

Margination

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Accumulation of leukocytes along vascular walls

Front 21

Function of selectins

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tethering of neutrophils and T cells to the endothelial wall

Front 22

Function of VCAM 1

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adhesion of lymphocytes, monocytes, eosinophils, and basophils

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What does E-selectin bind to?

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Glycoprotein on leukocyte

Front 24

What does L-selectin bind to?

Back 24

CD-34 on endothelium

Front 25

What does VCAM-1 bind to?

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Leukocyte VLA-4

Front 26

What does ICAM-1 bind to?

Back 26

LFA-1 on T cells

Front 27

Function of ICAM?

Back 27

anchors leukocytes to the endothelial cells

Front 28

Function of PECAM?

Back 28

transmigration of leukocytes between endothelial cells in vasculature

Front 29

What plays a crucial role in activating macrophage effector functions?

Back 29

IFN gamma

Front 30

Diseases mediated by DTH reactions

Back 30

- idiopathic uveitis
- inflammatory bowel disease
- insulin dependent diabetes
- acute cellular graft rejection

Front 31

Ocular conditions mediated by DTH reactions

Back 31

- corneal graft rejection
- cosmetic-induced conjunctivitis
- Behcet's disease
- sarcoidosis
- sympathetic ophthalmia

Front 32

Two mechanisms by which extracellular bacteria cause disease:

Back 32

1. Induce inflammation
2. Produce toxins

Front 33

Endotoxins

Back 33

In bacterial cell wall
Stimulate the production of cytokines by macrophages and other cells (vascular endothelial cells)

Front 34

Exotoxins

Back 34

Actively secreted by bacteria
(cholera, tetanus, diphtheria)

Front 35

Antibody isotypes involved in the immune response to extracellular bacteria

Back 35

IgM and IgG

Front 36

Mechanisms by which extracellular bacteria evade immunity (2)

Back 36

1. Secretion of substances which inhibit chemotaxis or complement proteins
2. Capsules which interfere with phagocyte binding and complement activation

Front 37

Major mechanisms of innate immunity to extracellular bacteria (2)

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1. Phagocytosis by neutrophils, monocytes, and macrophages.
2. Activation of complement

Front 38

How do viruses enter the host cell?

Back 38

By binding to cell surface molecules (rhinovirus - ICAM; HIV - CD 4, rabies - acetylcholine receptor)

Front 39

Cytopathic

Back 39

Interferes with normal cellular protein synthesis
Infected cell dies

Front 40

Non-cytopathic

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Proteins from virus become incorporated into MHC molecules on the cell surface and stimulate cytotoxic T cell activity

Front 41

Mechanisms of innate immunity in viruses (2)

Back 41

1. IFN released by infected cells
2. Lysis of infected cells by NK cells

Front 42

Principle mechanism for eliminating viral organisms

Back 42

Cell mediated immunity (action of cytotoxic T lymphocytes)
Recognize viral antigens in association with class I MHC antigens on the surface of any type of cell

Front 43

Mechanisms by which viruses evade host immunity (2)

Back 43

1. Change their appearance on a molecular level
2. Suppress immune response - attack immune cells & secrete immunosuppressive factors

Front 44

Toll-like Receptors

Back 44

Bind to different types of microbial molecules (flagellin, glycolipids, RNA, proteins, etc.), which stimulates cells to release cytokines

Front 45

Antibody isotype that responds to helminthic parasites

Back 45

IgE

Front 46

Main destructor cell in parasitic infection

Back 46

Eosinophil

Front 47

Allogenic graft (allograft)

Back 47

a graft transplanted between two genetically different individuals of the same species

Front 48

Xenograft

Back 48

a graft transplanted between a host and recipient of two different species

Front 49

Which grafts are not rejected?

Back 49

Autografts and isografts

Front 50

Which grafts are rejected?

Back 50

Allografts and Xenografts

Front 51

Immune response to allogenic antigen
(Direct Pathway)

Back 51

T cells, by way of their TCR's, crosss-react and directly bind to foreign MHC molecules on the surface of donor APC's, inducing their activation

Front 52

Immune response to allogenic antigen
(Indirect Pathway)

Back 52

An allogenic peptide derived from the donor is processed by recipient APCs and is presented to recipient T cells

Front 53

Mixed Lymphocyte Reaction (MLR)

Back 53

blood leukocytes from the recipient and donor are co-cultured. Donor cells are treated with anti-miotics.
Difference in the MHC alleles between the donor and recipient will cause the recipient's leukocytes to become activated and will proliferate. This response is measured by the amount of H-thymidine in the DNA of the replicating cells

Front 54

Function of CD4+ in an allogenic rejection

Back 54

secrete cytokines which helps propagate the MLR response

Front 55

Function of CD8+ in allogenic rejection

Back 55

lyse allogenic cells

Front 56

Hyperacute Rejection

Back 56

Alloantibodies bind to ABO blood group antigens on endothelial cells and activate complement, which releases thrombotic factors, causing vascular occlusion
Starves everything downstream of the thrombosis = kills the graft

Front 57

Acute Vascular Rejection

Back 57

alloantibodies bind to other antigens, such as MHC antigens, on endothelial cells and activate complement, causing immediate lysis of the cells.
CD8+ T cells also directly lyse non-MHC indentical donor endothelial cells

Front 58

Acute Cellular Rejection

Back 58

Parenchymal cells in the graft activate CD4+ cells which initiate a delayed type hypersensitivity reaction against non-MHC identical graft.
Direct lysis of parenchymal cells by CD8+ also occurs.

Front 59

Two approaches to delay or avoid rejection:

Back 59

1. Make the graft less immunogenic
- Match tissue and blood types
- Remove donor lymphocytes (passenger lymphocytes)

2. Suppress the recipient's immune system (cyclosporin)

Front 60

Graft versus host disease (GVH)

Back 60

allogenic donor lymphocytes react against host tissues in an immunologically compromised host

characterized by lymphocytic infiltration of the skin, liver, and GI tract

Front 61

How do cyclosporin and tacrolimus work?

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Inhibits T cell activation by blocking IL-2 production

Front 62

How does rapamycin work?

Back 62

Blocks T cell proliferation by inhibiting IL-2 cell signaling

Front 63

Carcinomas

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cancers derived from epithelial cells

Front 64

Sarcomas

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tumors arising from bone, cartilage, and fat

Front 65

Lymphomas

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tumors of the lymphoid tissue

Front 66

Leukemias

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marrow and blood-borne malignant tumors of lymphocytes and other hematopoietic cells

Front 67

Teratoma

Back 67

a tumor derived from a mixture of tissues

Front 68

Adenomas

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benign epithelial tumors

Front 69

Oncofetal antigens

Back 69

normally expressed in high levels on fetal tissue and low levels on adult tissue

do not cause an immune response

measuring levels of these antigens is useful in diagnosis

Front 70

Which protein is elevated in hepatocellular carcinoma?

Back 70

alpha-feto protein (AFP)

Front 71

Which protein is elevated in colon cancer?

Back 71

carcinoembryonic antigen (CEA)

Front 72

Which immune cells are not immunologically restricted?

Back 72

NK cells

Front 73

Which cytokine mediates the direct and indirect killing of tumor cells by macrophages?

Back 73

TNF

Front 74

Antigenic modulation

Back 74

the loss of surface expression of tumor antigens as a result of the internalization of the antigen-antibody complex

Front 75

Immunosuppressive factor secreted by some tumors

How does it work?

Back 75

TGF-beta

inhibits T and B cell function

Front 76

More people die from this type of cancer than any other type

Back 76

Lung cancer

Front 77

p53 gene function

Back 77

Tumor suppressive gene
Binds to DNA to initiate its repair
Mutated p53 can lead to cancer

Front 78

Adenomatous Polyposis Coli (APC)

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Tumor suppressive gene
Mutations can cause colon cancer

Front 79

BRCA-1 and BRCA-2

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Tumor suppressive genes
Mutations cause breast cancer

Front 80

Tamoxifen

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Estrogen receptor blocker

Prevents breast cancer recurrence

Front 81

Conditions encoded by oncogenic viruses

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- Epstein-Barr virus
- Human papilloma virus
- Human herpes simplex virus 8
- Hepatitis B virus
- Human T lymphotropic virus (RNA virus)

Front 82

FasL

Back 82

mechanism by which tumors evade immune system

tumors express FasL which binds to Fas on T cells, resulting in T cell apoptosis

Front 83

High doses of this prevents the proliferation of tumor cells

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IL-2

Front 84

Poly ADP Ribose Polymerase (PARP)

Back 84

possibly used in the treatment of ovarian and breast cancer

enzyme involved in reparing single strand DNA breaks in BRCA mutations

blocking this enzyme would cause the cancer cell to undergo apoptosis

Front 85

Mimicry

Back 85

once the body is exposed to a particular antigen, it begins attacking a self cell which expresses an antigen that looks similar to the foreign antigen

Front 86

What diseases are caused by mimicry?

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Thyroiditis and Grave's disease

Front 87

What causes myasthenia gravis?

Back 87

a failure to delete self reactive clones. These clones attack self acetyl choline receptors.

Front 88

Mechanisms by which autoimmunity develops (4)

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1. Failure to delete self-reactive clones in the thymus
2. Mimicry
3. Exposure of previously concealed self antigens
4. By pass regulatory mechanisms -- polyclonal activation by LPS

Front 89

X-linked agammaglobulinemia

Back 89

absence of gamma globulin in the blood

patients with this disease have reduced or entirely missing B cells

Front 90

DiGeorge Syndrome

Back 90

congenital malformation of the thymus --> defective maturation of T cells

usually normalize by age 5 through the growth of a thymus-like tissue

nude (athymic) mouse

Front 91

Severe combined immunodeficiencies (SCID)

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defective development of T and B cells

Front 92

Transfection

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gene replacement therapy -- normal gene is linked to the nucleic acid from a non-pathogenic virus which facilitates the gene's entry into the host genome

Front 93

Adenosine deaminase
(ADA)

Back 93

Enzyme required for the normal metabolism of purines in lymphocytes.
Absence of this enzyme results in accumulation of toxic metabolites which destroy the cell.

Front 94

A mutation in what gene causes Leber's congenital amaurosis?

Back 94

RPE65

Front 95

During HIV infection, what binding causes a conformational change?

Back 95

Binding of gp120 to the CD4 molecule on the cell surface

Front 96

What binding allows for the transfer of the HIV viron into the cell?

Back 96

Binding of gp120 to CXCR4

Front 97

HIV nef protein

Back 97

mechanism of evading immune detection

downregulates MHC class I molecules from the infected cell's surface --> reduced capacity of the cell to stimulate T cell mediated lysis

Front 98

Function of Azidothymidine (AZT)

Back 98

reverse transcriptase inhibitor

Front 99

Drug that reduces the transmission of HIV from an infected mother to her unborn child

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Azidothymidine (AZT)

Front 100

HAART (highly active anti-retroviral therapy)

Back 100

combination drug of protease inhibitors and reverse transcriptase inhibitors

Front 101

Function of protease inhibitors

Back 101

inhibit the proteases required for the packaging of new virions for release from the infected cell

Front 102

Side effects of HAART (3)

Back 102

- dyslipidemia
- insulin resistance
- premature atherosclerosis

Front 103

Enfuvirtide

Back 103

prevents HIV from fusing with its target cell by blocking gp41

Front 104

Selzentry

Back 104

prevents HIV from fusing with its target cell by blocking the chemokine receptor

Front 105

Isentress

Back 105

blocks HIV from integrating into the host genome

Front 106

What is the most commonly observed ocular abnormality in AIDS patients?

Back 106

Cotton wool spots

Front 107

In 1995, the discovery of which class of drug significantly decreased the death toll of HIV patients?

Back 107

Protease Inhibitors

Front 108

Immunological effects of TGF-beta in the eye

Back 108

Inhibits T, B, and NK cell activity

Inhibits the development of cytotoxic T cell and cytokine production

Front 109

ACAID

Back 109

Suppresses DTH and complement-fixing antibodies

Front 110

Where does ocular melanoma tend to metastasize to?

Back 110

The liver

Front 111

Leukocoria

Back 111

loss of red reflex

happens in retinoblastoma

Front 112

What layer of the tears is IgA localized to?

Back 112

Mucin layer

Front 113

Lactoferrin

1. Produced by?

2. Function?

Back 113

1. Produced by acinar cells

2. Binds iron, which is required for bacterial growth

Front 114

Lysozyme

1. Function?

Back 114

cleaves the cell wall of gram positive bacteria

Front 115

Function of Beta lysin

Back 115

disrupts bacterial cell wall and inhibits catalase and peroxidase