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Immunology Final > Dysregulation & Deficiency > Flashcards

Dysregulation & Deficiency Flashcards

1
Q

About how much of the world’s population is infected with TB?

A

1/3

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2
Q

Where in the normal immune response does TB go wrong?

A

TB organism modifies on surface of phagosome instead of fusing with lysosome and being destroyed

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3
Q

When the TB organism kills the macrophage during its escape, how does it harm the host?

A

Necrotic debris from killed macrophage are released into lung tissue (inflammatory response) leading to tissue damage

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4
Q

What are cathelicidins?

A

Antimicrobial enzymes whose release is stimulated by vitamin D

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5
Q

How does one recover from TB and then live with the chronic infection?

A

1 INF-gamma hyperactivates macrophages which are able to deal with TB organism
2 Macrophages and other cells (neutrophils) eliminate invader
3 T cells come into play
4 Vitamin D stimulates release of antimicrobials (cathelicidins)

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6
Q

When does sepsis occur?

A

When chemicals released into bloodstream to fight infection trigger inflammation throughout body

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7
Q

How can sepsis lead to death?

A

Multiple organ failure, septic shock leading to dropped BP then death

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8
Q

Sepsis is most serious in what group of people?

A

Elderly or immunocompromised

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9
Q

Is sepsis not an issue in the U.S.?

A

Still is: 250,000 die per year

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10
Q

What major cytokine is involved in sepsis, and what is its effect?

A

TNF; increased vascular permeability, fluid loss, decreased blood volume and BP, septic shock and heart failure

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11
Q

How does vagal stimulation affect macrophage release of TNF?

A

Inhibitition

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12
Q

Allergies are typically associated with which helper T cell bias?

A

2

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13
Q

Non-allergic people produce more of which antibody?

A

IgG

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14
Q

What helper T cell bias is associated with non-allergic people?

A

Th1

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15
Q

What causes allergies?

A

Overproduction of IgE antibodies

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16
Q

Th2 cells involved in an allergic response secrete which cytokine to recruit many eosinophils from the bone marrow?

A

IL-5

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17
Q

Which cells play a prominent role in the delayed allergic phase?

A

Eosinophils

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18
Q

What is the normal function of mast cells, basophils, and eosinophils?

A

Provide defense against parasitic infection that are too large to be phagocytized by macrophages and neutrophils

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19
Q

When is the only time that mast cells, basophils, and eosinophils SHOULD degranulate?

A

In response to IgE binding to parasite, limiting collateral damage in tissues

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20
Q

Why is the fetus representative of a Th2 bias?

A

Half the fetus is paternal and could be seen as foreign by the mother so this provides protection

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21
Q

What makes up the Th1 subset of cytokines?

A

TNF, IL-2

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22
Q

What is the function of TNF?

A

Activate NK cells

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23
Q

What is the function of IL-2?

A

Proliferation of NK cells and CTLs

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24
Q

What is the role of the placenta when it comes to helper T cell bias?

A

Produces large quantities of IL-4 which causes both maternal and fetal helper T cells to become Th2

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25
Q

It is advantageous to bias the fetus AWAY from which helpter T cell bias?

A

Th1

26
Q

What is thought to shift the newborn back to a Th1 bias after birth?

A

Contact with soil microbes and early childhood infections (possible allergy prevention)

27
Q

What is the relationship because location of upbringing as a child and incidence of allergies/asthma?

A

Farm life - lower incidence
City life - higher incidence
(also lower incidence when growing up with dogs)

28
Q

If one identical twin has allergies, what is the likelihood for the other to develop the same ones?

A

50%

29
Q

What kind of people are more likely to have inherited particular class II MHC genes?

A

Atopic (allergic) people

30
Q

What cytokine is responsible for class switching to IgE thus having an impact on over-abundance of allergic reactions?

A

IL-4

31
Q

How do glucocorticoids (cortisol) work to treat allergies?

A

Block cytokine production by Th cells activating fewer B cells

32
Q

What is the downside to using glucocorticoids as treatment for allergies?

A

Increased susceptibility to infectious disease and immunosuppression

33
Q

What treatment for allergies functions to block the binding of IgE to mast cells?

A

Xolair (Omalizumab)

34
Q

What is the downside to Xolair for treating allergies?

A

Crazy expensive ($1000 per month)

35
Q

How do Claritin and allegra work to treat allergies?

A

Block histamine (H1)

36
Q

How do infections of gradually increasing doses of crude extracts of allergens work to treat allergies?

A

Patient become tolerant because B cells class switch from IgE to another like IgG (iTregs are generated to produce cytokines like IL-10 that suppress IgE production)

37
Q

What cytokines are associated with a Th2 bias?

A

IL-4, IL-5, and IL-13

38
Q

Autoimmune disease affected what percentage of the U.S. population?

A

5-7.5% (15-23 million Americans)

39
Q

Autoimmune disease is more common among which gender?

A

Women

40
Q

About how many known autoimmune disease are there?

A

100

41
Q

How much more common are autoimmune diseases now than just several decades ago?

A

3X

42
Q

Molecular mimicry can lead to what serious immune system issue?

A

Autoimmune disease (if natural guards are broken)

43
Q

There may be a link between Myasthenia gravis and what virus?

A

Polio virus

44
Q

Which type of antibody complexes can activate macrophages leading to chronic inflammation in Rheumatoid arthritis?

A

IgM-IgG

45
Q

What condition is a result of the immune system attacking the myelin of the PNS?

A

Guillain-Barre

46
Q

What is transverse myelitis?

A

Inflammatory process of the spinal cord that can cause axon demyelination

47
Q

What is autoimmune lymphoproliferative syndrome?

A

Genetic defect where T cells refuse to die when chronically stimulated by self antigens (defect in apoptosis due to defect in Fas or Fas ligand proteins)

48
Q

What 3 things must be necessary to develop an autoimmune disease?

A

1 must have MHC molecules that can present self-antigen
2 must have T lymphocytes and some B lymphocytes with receptors to recognize self antigens
3 environmental factors leading to breakdown of tolerance mechanisms for self-reactive lymphocytes

49
Q

Autoimmune diseases frequently follow what conditions?

A

Bacterial or viral infections

50
Q

What is probably one of the key environmental factors that triggers autoimmune disease (along with environmental pollutants and possibly chronic inflammation)?

A

Bacterial or viral infections

51
Q

Can molecular mimicry alone cause an autoimmune disease?

A

No; must also be an inflammatory reaction going on in the same tissues that express self antigen

52
Q

What is the result of a mutation leading to a nonfunctional CD40 (B cell) or CD40L (Th cell)?

A

B cells unable to class switch and secrete mainly IgM

53
Q

What condition is the result of a malformation and dysfunction of the thymus, and what is the problem with it?

A

DiGeorge Syndrome (thymic tissue missing –> no T cell function)

54
Q

What is the problem with severe immunodeficiency syndrome (SCIDS)?

A

Neither B cells nor T cells function due to defected protein that is required to produce BCR and TCR

55
Q

What cells are primarily targeted by AIDS?

A

Helper T cells (but also macrophages, dendritic cells, CD4 protein)

56
Q

What is usually the cause of death in those with AIDS?

A

Opportunistic infections that the body can’t fight off (examples = Kaposi sarcoma, pneumocytis carinii)

57
Q

Why is HIV-1 able to defeat the immune system in many cases?

A

It is a slowly replicating lentivirus (retro RNA virus) that sits in a latent state and is undetected by CTLs
Also, high mutation rate

58
Q

What is the drug treatment for AIDS?

A

Highly Active Anti-Retroviral Treatment (HAART) of nucleoside/tide reverse transcriptase inhibitors to inhibit high mutation rate

59
Q

The innate immune cells in the less than 1% of those able to control their HIV infection secretion more of which substances?

A

IFN-alpha and IFN-beta

60
Q

What else is different in the small percentage of those who can control their HIV infection?

A

More efficient MHC molecules to present HIV-1 peptides and activate CTLs earlier, more vicious CTLs, quicker responses overall

Immunology Final (6 decks)

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