Immunology - Immune Responses To Infections

Front 1

What is an agent that kills bacteria?

Back 1

Bactericidal

Front 2

What is a bacteriostatic agent?

Back 2

Slows bacterial growth

Front 3

Cryptococcus neoformans

Back 3

- Polysaccharide Encapsulated fungal infection
- Immunosuppressant patients are susceptible b/c need CD4+ cytokines (IFNγ) to kill it

Front 4

Mycobacterium tuberculosis

Back 4

- Intracellular bacterium, causes tuberculosis
- inhibits fusion of the phagosome/endosome with lysosomes

Front 5

Rickettsia rickettsii

Back 5

- Escapes to the phagocyte cytosol
- Causes Rocky Mountain Spotted Fever
- Can be phagocytosed

Front 6

Shigella dysenteriae

Back 6

Shiga Toxin - destroys endothelial cells and macrophages = bloody diarrhea
- Shigella Dysentery


- bind to M cells and are endocytosed
- lyse the endosomal wall and enter cytoplasm
- spread laterally to infect adjacent cells
- some are phagocytosed – toxin destroys the macrophages

Front 7

Streptococcus pneumoniae

Back 7

has polysaccharide capsule
- causes bacterial pneumonia
- not presented to CD4+ cells = no T-cell activated (T-independent antigen)
- Extracellular bacteria

Front 8

Borrelia burgdorferi

Back 8

VlsE (variable major protein-like
sequence expressed
- millions of variants
- infections can last for months

Front 9

Candidiasis Albicans

Back 9

- part of human flora
- opportunistic - only affects immunodeficient
- binds to glycoproteins in secretions of mucus membranes
- causes Candidiasis (yeast infections) - Vaginal and Oral

Front 10

HIV

Back 10

- destroys CD4+ T-cells
- ↓ Cytokines = vulnerable to opportunistic infections
-gp120 binds to CD4+, conformational change = exposes binding site to CCR5 and CXCR4
- Binds to CCR5 and CXCR4 on T-cell, Dendritic or Macrophage
- forms a syncytia formation - huge conglomerate of CD4+ cells. fuse together on gp120 spikes.

Front 11

What is another name for fungal infections?

Back 11

Mycoses

Front 12

Which type of cells do intracellular bacteria often thrive within? Why?

Back 12

Macrophage phagosomes, because they have evolved mechanisms to evade the proteolytic degradation that occurs within the phagocytic vacuole.

Front 13

How do extracellular bacteria become pathogenic?

Back 13

By hindering phagocytosis with their polysacharide capsule.

Front 14

What are extracellular bacteria vulnerable to within the host environment?

Back 14

The soluble mediators of the immune system.

Front 15

What is the primary means of destruction for extracellular bacteria? How is this enhanced?

Back 15

Phagocytosis.
-It is enhanced by activation of B-cells, T-cells and complement.

Front 16

Name three ways that antibodies contribute to the destruction of extracellular bacteria.

Back 16

1. They activate the classical pathway of complement.
2. Serve as opsonins for opsonin mediated phagocytosis.
3. May also bind to toxins and neutralize them.

Front 17

What does an immune response to viruses depend on?

Back 17

The site where the virus is detected and whether the infection is primary or secondary.

Front 18

Where do viruses have to be found in order to be phagocytosed?

Back 18

Blood, lymph or interstitial fluid.

Front 19

Why is phagocytosis of viral particles not the primary way of destroying the infection?

Back 19

Because they are only found in fluids for a transient period during the initial infection when they are released from infected cells

Front 20

How are viruses primarily eliminated?

Back 20

The infected cell has to be destroyed by NK cells and CTL.

Both release lytic granules following conjugate formation within the infected cell.

Front 21

How are NK cells different from CD8+ T-cells?

Back 21

NK Cells
- can deliver lethal hit immediately
- Broad specificity (can bind to anything with FcγR)
- Inhibited by too much class I MHC
- IL-2 enhances

CD8+ T-cells
- need to differentiate pCTL → CTL to deliver lethal hit (requires IL-2, IFNγ)
- very specific. must be on the class I MHC
- upregulated by class I MHC
- IL-2 is required

Front 22

Where do extracellular bacteria usually adhere to as a preliminary step to tissue invasion?

Back 22

Mucus membranes like: nasopharynx, respiratory, genitourinary or GI tracts.

Front 23

What might bacteria that encounter mucosal membranes be stopped by?

Back 23

Lactoferrin, a protein that binds iron, reducing the amount of available to bacteria so that they are unable to grow.

Front 24

What is a better protective barrier, skin or mucosal membrane?

Back 24

Skin

Front 25

What happens if bacteria get passed the skin and mucous membranes?

Back 25

They go to the interstitial fluid, blood or lymph.

In order to survive here, they have to stop the innate immune system.

Front 26

What is an opsonin?

Back 26

host protein that binds to a bacteria and is recognized in a specific manner leading to phagocytosis

Proteolytically derived complement proteins or IgG antibodies.

- IgG - secreted by B cell (plasma cell)
- C3b - complement protein
- C-reactive Protein - secreted by IL-6

Front 27

When does opsonin mediated phagocytosis typically occur?

Back 27

Only after the complement system has been activated or after B cells differentiate into plasma cells secreting IgG antibodies.

Front 28

What are reactive oxygen intermediates, nitric oxide and reactive nitrogen intermediates also known as?

Back 28

Bactericidal agents.

Front 29

What are the two roles of the complement system in the elimination of bacteria?

Back 29

1. Proteolytically derived complement fragments serve as opsonins.

2. The generation of a membrane attack complex and its insertion into the bacterial cell surface causes the destruction of the bacterium by osmotic lysis.

Front 30

What does B cell activation require?

Back 30

CD4 +T cells and the cytokines they secrete.

Front 31

What is a notable feature of Mycobacterium tuberculosis?

Back 31

The formation of granulomas

Front 32

What is a granuloma?

Back 32

An aggregation of macrophages surrounded by CD4+T lymphocytes secreting Type 1 cytokines, particularly IFNγ

Front 33

What is an “opportunistic” fungi? Why is it called this?

Back 33

Fungi that are part of the normal flora, or are wide spread in the environment are called this because they are relatively harmless to healthy hosts.

Front 34

Are opportunistic fungi likely to cause infections?

Back 34

NO, but non-opportunistic ones are.

Front 35

How are fungal infections usually eliminated? How is this enhanced?

Back 35

By phagocytosis. It is enhanced in the presence of opsonins.

Front 36

What does immunity to Candida albicans require?

Back 36

Activation of both B cells and CD4+ T cells.

Front 37

What happens if the hyphae of the fungi are too large for neutrophils to destroy?

Back 37

neutrophils can destroy them by secreting proteolytic molecules into microenvironment

- neutrophils attach to fungi to make sure metabolites are within range

Front 38

What protects the Streptococcus pneumoniae bacteria from phagocytosis? Until when?

Back 38

The presence of a polysaccharide caspule.

Until B cells are activated and IgG opsonins are produced.

Front 39

Why is each infection with the Streptococcus Pneumoniae potentially life-threatening?

Back 39

Since it is T-cell independent, no memory cells are made
→ therefore each infection takes days for IgG antibodes to be made and serve as opsonin

Front 40

Which virus encodes a viral IL-10-like molecule that inhibits the development of effective anti-viral cytotoxic T cells needed to kill virally infected cells?

Back 40

Epstein Barr Virus, EBV: causes mononucleosis.

Front 41

What is the receptor for the CXC chemokine?

Back 41

Stromal cell-derived factor 1 (SDF-1)

Front 42

Why is it good that HIV enters through bodily fluids and not directly into a cell?

Back 42

Because this provides a small window of opportunity for HIV specific B cells to be activated, providing there is sufficient T cell help.

Front 43

What do the B cells do once HIV is detected? What does this do?

Back 43

Antibodies are made.

these antibodies can be detected = HIV+.
- these antibodies only fight free viral peptides = not protective anti-viral immunity

Front 44

How are uninfected CD4+ T cells destroyed by HIV?

Back 44

- Infected CD4+ T cells interact with viral proteins - form syncytia formation.
- Uninfected cells are fused in the syncytia and both cells are destroyed

Front 45

What is a useful marker for disease progression in AIDS?

Back 45

CD4 T cell numbers decline

Front 46

How long does it take for HIV infection to reach a steady state?
How long does the patient have to live after the steady state is reached?

Back 46

Steady state – 6 mo
1 year - 15 years

Front 47

If an air-borne bacteria escapes coughing and alveolar macrophages, how does it get into the lung?

Back 47

1. It binds to epithelial cells and enters the lungs by transcytosis through the epithelial cells.

2. Or it may enter inside a macrophage (“trojan horse”) as the macrophage enters.

Front 48

How is tuberculosis tested for?

Back 48

purified protein derivative (PPD) from Mycobacterium tuberculosis (skin test)

- Cutaneous reaction develops from reactivation of memory CD4+T cells at site of infection

- referred to as the delayed-type-hypersensitivity (DTH) reaction or the Mantoux reaction.

Front 49

How do food borne/oral-fecal intracellular bacteria get in?

Back 49

1. They can get in by binding to M cells.

2. M cells are interspersed between epithelial cells and don’t have a protective mucous covering.
They pass through M cells in vesicles and go to the lamina propia where they can be phagocytosed.

3. They can also go to the mesenteric lymph nodes if they leave the lamina propra. IF they resist degradation by macrophages, they can proliferate in them.

Front 50

Where is Candida albicans found primarily?

Back 50

In the oral cavity and female genital tract.
- bind to glycoproteins in secretions of mucus membranes on epithelial surface

Front 51

How might Candida albicans get to the basement membrane and below?

Back 51

By forming budding protrusions termed “hyphae”.