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Host Defense Exam 2 > Perturbations in the Super System > Flashcards

Perturbations in the Super System Flashcards

1
Q

What are superantigens?

A

antigens produced by bacteria and viruses that overstimulate the immune system and lead to cytokine storm

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2
Q

How do superantigens interact with the immune system?

A

rather than being take up, processed, and presented via MHC to T cells (in the way normal antigens would), superantigen interact with the “side” of the MHCII-TCR complex

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3
Q

What are some examples of superantigens?

A

toxic schock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin (SE)

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4
Q

What is a cytokine storm?

A

polyclonal overactivation of T cells, resulting in a large release of INF-gamma,

which overactivates macrophages, which produce large amounts of IL1, 6, and TNF-alpha, which leads to a

increase in capillary permeability
decrease in blood pressure
fever
rash (especially on palms and soles)
disseminated intravascular permeability
shedding of the skin (desquamation)
multi organ failure
coma
death
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5
Q

What is the intensity of the response to a superantigen depedent on?

A

highly dependent on the polymorphism of the hosts MHC classII

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6
Q

What is the advantage of overactivating the immune system, from the pathogens point of view?

A

highly activated immune effector cells will undergo widespread apoptosis and thus be unable to respond to the invading microorganism, which then uses the host for propagation prior to the death of the host

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7
Q

What can polymorphic MHCII and differential expression of TCR lead to?

A

increased susceptibility to disease

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8
Q

What does a polymorphism in CCR5 lead to?

A

increased resistance to HIV

decreased resistance to west nile

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9
Q

What does HIV need to enter the cell?

A

CD4 receptor and the chemokine receptor CCR5

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10
Q

What is CCR5 a receptor for?

A

chemokines expressed on immune effector cells

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11
Q

What does ligation of CCR5 do?

A

ligation of CCR5 on T cells by chemokines leads to directed leukocyte migration to the site of inflammation, permitting an immune response to antigens

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12
Q

What do individuals who are homozygous and heterozygous for the polymorphism in CCR5 (CCR5-delta32) have?

A

homozygous - complete resistance to HIV

heterozygous - slow progressors of HIV

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13
Q

What does west nile cause?

A

viral encephalitis

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14
Q

What is protection from west nile dependent upon?

A

accumulation of CCR5+ leukocytes, including CD4+, CD8+. CD14+, CD56+

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15
Q

What are some (5) ways viruses evade the immune system?

A

induce production of inhibitory cytokines such as IL-10 or produce IL-10 orthologs (vIL-10)

encode chemokines or induce the production of chemokines that attract susceptible cells to the site of inflammation, providing new material for the virus to infect

encode chemokine receptors that facilitate migration of cells to different parts of the host, facilitating the spread of the virus

alter the activity of host chemokine receptors, preventing immune activation or migration

induce host chemokine receptor internalization, preventing infected cell from responding to chemokine signals

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16
Q

Why would a virus induce the production of IL-10?

A

reduces inflammatory cytokines such as IFN-gamma, and impairs CD4+ Th1 activation, shifting the balance from Th1 to a Th2 response, which interferes with CD8 T cell killing and inhibits Ab production

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17
Q

What causes autoimmune diseases?

A

self-reactive T and B lymphocytes

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18
Q

how common are autoimmune diseases?

A

3rd highest cause of morbidity and mortality in developed countries after cardiovascular disease and cancer

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19
Q

What probably plays a role in the development of autoimmune disease?

A

inheritance and gender

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20
Q

What gender is affected more, and what does this suggest?

A

females, which suggests that sex hormones modulate immunity and the clinical expression of autoimmunity

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21
Q

What are some examples of differences in the immune system between males and females?

A

females have a more vigorous Th1 response (except during pregnancy)

females have a more vigorous Ab response (except during pregnancy)

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22
Q

What does autoimmunity result from?

A

a loss of tolerance

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23
Q

What does normal immunity depend on?

A

the ability to differentiate between self and non-self, and to maintain tolerance to self

24
Q

What kind of process is tolerance?

A

it is learned and active process

25
Q

What are the major two ways that T cell tolerance to self is enforced?

A

central and peripheral

26
Q

What is central tolerance dependent on?

A

the Thymus

27
Q

How does central tolerance occur?

A

negative selection and clonal deletion of self-reactive thymocytes

28
Q

What is another major intrathymic tolerance mechanism?

A

AIRE gene complex

29
Q

Where is AIRE located?

A

medullary thymic epithelium

30
Q

What does AIRE do?

A

present a myriad of tissue peptide antigens (especially neural and endocrine) on the thymic epithelium

31
Q

What are the two responses to an interaction with AIRE produced Ag?

A

High affinity TCR reaction deletes the T cell

low affinity TCR reaction results in the production of a Treg (FoxP3 expression)

32
Q

What does a mutation in AIRE result in?

A

autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECD)

33
Q

What kind of tolerance is peripheral tolerance?

A

active, Ag specific process

34
Q

What mediates peripheral tolerance?

A

enforced by CD4+, 25+ FoxP3+ Treg cells that prevent autoattacks by self reactive thymocytes that have escaped the thymus

35
Q

Contrast B cell tolerance to T cell tolerance

A

negative deletion is not as stringent for B cells during development in the bone marrow as it is for T cells in the thymus

36
Q

When may self-reactive B cells develop?

A

during Ag driven somatic hyper-mutation in the periphery

37
Q

What happens to most self-reactive B cells?

A

the die from neglect or are suppressed by CD4 25 FoxP3 Tregs

38
Q

what can happen if self-reactive B cells go unchecked?

A

can produce Ab that block functions of cells, accelerate cell functions by mimicking agonists, or promote cytotoxic responses

39
Q

What are the two classes of autoimmune diseases in terms of specificity?

A

organ specific and systemic

40
Q

What are some examples of an organ specific autoimmune disease?

A

Insulin dependent diabetes mellitus (IDDM) - type I diabetes

Graves’ disease

Goodpasture’s syndrome

Myasthenia gravis

Multiple sclerosis

41
Q

What is the etiology of IDDM and what organ is affected?

A

Pancreas: CD8 and Ab respond to beta cells resulting in beta cell destruction

42
Q

What is the etiology of Graves’ disease and what organ is affected?

A

Thyroid: Ab to TSH receptor resulting in excess thyroid hormone production and hyperthyroidism

43
Q

What is the etiology of Goodpasture’s syndrome and what organ is affected?

A

Lung and Kidney: Ab to type IV collagen in alveolar and glomerular basement menbranes resulting in pulmonary hemorrhage and glomerulonephritis

44
Q

What is the etiology of Myasthenia gravis, and what organ is affected?

A

Neuromuscular: Ab to nicotinic acetylcholine receptor, which is present on skeletal muscles and at neuromuscular junctions. The Ab blocks neurotransmission resulting in muscle weakness

45
Q

What is the etiology of Multiple sclerosis and what organ is affected?

A

Brain: CD4 is reactive with myelin basic protein which results in demyelination

46
Q

What are two examples of a systemic autoimmune disease?

A

Systemic lupus erythematosus

Rheumatoid arthritis

47
Q

What is the etiology of systemic lupus erythematosus, what are the symptoms, what is the laboratory diagnosis, and what is affected?

A

Basement membrane: auto-Ab to many auto-Ag, but especially ds-DNA which results in immune complex deposition on basement membranes with the activation of complement and inflammation

results in malar rash (butterfly rash), musculoskeletal pain, and renal problems (glomerulonephritis - hallmark)

laboratory diagnosis: Anti-nuclear Ab, Anti ds-DNA, C3 levels decreased

48
Q

What is the etiology of rheumatoid arthritis, and what is affected?

A

Joints: CD4 response that stimulates an inflammatory response in the synovial membrane of joints and the articular surfaces of cartilage and bone

CD4 T cells activate B cells, macrophages, and plasma cells

cytokines induce production of MMPs and RANK ligand by fibroblasts

49
Q

What are the classes of autoimmune diseases in terms of effector mechanisms?

A

Type II, III, and IV

50
Q

What is type II autoimmunity, what is the primary effector mechanism, and what are some examples of diseases that fit under this category?

A

Type II hypersensitivity: Ab against cell surface or ECM antigens

IgG is the primary effector mechanism

Graves’, Goodpasture’s, Myasthenia gravis

51
Q

What is type III autoimmunity, what is the primary effector mechanism, and what are some examples of diseases that fit under this category?

A

Type III hypersensitivity: formation and deposition of immune complexes

Immune complexes are the primary effector mechanism

systemic lupus erythematosus

52
Q

What is type IV autoimmunity, what is the primary effector mechanism, and what are some examples of diseases that fit under this category?

A

Type IV hypersensitivity: T Cell mediated

T cells are the effector mechanism

IDDM, Rheumatoid arthritis, Multiple sclerosis

53
Q

What else can pancreatic beta cells be destroyed by?

A

infectious agents such as mumps virus, rubella virus, coxsackie B virus

toxic chemicals

54
Q

What do most pts with RA have and what does it result in?

A

85% have rheumatoid factor: IgM, IgA, and IgG specific for IgG

this results in immune complex formation and inflammation

55
Q

What is MS characterized by and where is it most prevalent?

A

patches of demyelination and inflammation of the myelin sheath

highest prevalence in the northern hemisphere

56
Q

What are some major risk factors for autoimmune disease?

A

genetic (HLA type)

female

environmental (smoking with rheumatoid arthritis)

infection

Host Defense Exam 2 (11 decks)

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