Week 10: Host Defense Flashcards

1
Q

innate immunity

A

• Physical and chemical barriers that exists to prevent infection from occurring in the first
place
• Non-specific, primary response mechanisms

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2
Q

adaptive immunity

A

• Highly coordinated and specific response to a particular pathogen

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3
Q

Anatomical Barriers:

A
Physical
• Skin
• Mucus
• Cilia
 Chemical
• Stomach acid
• Enzymes in tears
• Gland secretions
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4
Q

Pattern recognition receptors (PRR)

A
recognize structures that are
shared by a class of microbes
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5
Q

Toll-like receptors (TLRs),

A

expressed on Macrophages and Dendritic cells,

recognize different classes of microbial structures; 10 unique TLRs exist;

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6
Q

When PRRs recognize their target molecule,

A

the macrophage or the dendritic cell will

release cytokines into the environment.

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7
Q

The cytokines released by a macrophage or dendritic cell are specific
to

A
the type of PRR that was triggered, and thus is specific to the type/
class of pathogen.
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8
Q

Interferons

A

signal to neighbouring cells that a viral infection is present. This shuts down
the neigbouring cells’ ability to synthesize proteins so that viral replication is inhibited
and spread is slowed in the area

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9
Q

If the innate response isn’t sufficient to reduce the infection,

A

the

adaptive response is activated

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10
Q

The bridge between the innate and the adaptive immune response
are the

A

antigen presenting cells (APCs).

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11
Q

Now loaded with antigen,
the APC must present
antigen to a

A

lymphocyte to
stimulate an adaptive
response

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12
Q

T cells develop from

A

lymphocyte precursor cells in the bone marrow

and complete their maturation in the thymus (hence, T-cell)

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13
Q

There are two types of T-cells

A
  • Th cells – Helper T-cells

* Tc cells – Cytotoxic T-cells

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14
Q

If the TCR recognizes the antigen,

A

the

Th cell is activated

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15
Q

Upon activation Th cells

A
Proliferate
Begin to produce effector cytokines that
support either the
• Cell-mediated response
• Humoral response
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16
Q

For intracellular pathogens (viruses, intracellular bacteria)

A

Th cells will release IL-12, among other cytokines, which will activate Tc cells

17
Q

Upon activation, Tc cells

A

• Proliferate
• Circulate through the body and scan all
cells for antigen
• When the TCR recognizes its specific
antigen, it kills the infected host cell to
prevent further spread

18
Q

Upon activation, most Th and Tc cells become

A

effector T-cells;

however, some become memory T-cells

19
Q

Effector T-cells

A

Elicit the primary response and mediate their effects immediately

20
Q

Memory T-cells

A
  • Do not respond immediately; are mostly inactive

* Long lived cell

21
Q

B cells develop from

A

lymphocyte precursor cells in
the bone marrow and complete their maturation in
there as well

22
Q

B-cells require two signals to

activate it

A

• Specific antigen-antibody interaction
• Cytokines secreted by Th cells;
generally IL-4 and IL-5

23
Q

Activated B-cells will proliferate and

develop into either:

A

• Effector B-cells; called plasma cells
which secrete antibodies
• Memory B-cells; long-lasting cells

24
Q

Neutralization

A

• Binds to the surface of pathogens, effectively

blocking their access to infect other cells

25
Agglutination
• Because antibodies have two binding sites, they can bind to two antigens. Clumping of several antibody-antigen complexes is called agglutination • Pathogens stuck in these clusters are unable to infect host cells
26
Opsonization
• Antibodies have a binding site for phagocytic cells; as a result they enhance phagocytosis of antibody-bound antigens
27
IgM
Initial antibody secreted by plasma cells
28
IgG
• Follows IgM production, but is the type that is most abundantly produced during a humoral response • Due to its size it can cross the placenta and enter breast milk; important in newborn immunity
29
IgA
* Offers protection in the mucous membranes * Tears, saliva, GI tract * Can also enter into breast milk for newborn immunity
30
IgE
• Most often associated with allergy
31
inductive period
time between the initial infection and the onset of the adaptive response (usually measured by antibody production)
32
Regulatory T-cells (Tr cells) help to slow the adaptive | response after an infection is cleared
• Effector T-cells and plasma cells (effector B-cells) are eliminated • Memory T-cells and memory B-cells persist
33
A secondary exposure to the same pathogen typically results in
faster and stronger response due to the presence of Memory T cells and B cells
34
Inactivated, or Heat-killed vaccine
* Made from killed pathogen * Generally develops a weaker response and less protection * Regarded as highly safe – no chance of mutation
35
Attenuated
• Made from weakened pathogens • Generally develops a more robust response, more memory cells and better long-term protection; but, in some cases they are regarded as less safe. Since it is a live, albeit weakened, form of the pathogen there is always a slight risk that mutation could result in infection
36
Subunit
* Made from subunits of the pathogen (antigens/ proteins) * Generally develops a weaker response and less protection * Regarded as highly safe – no chance of mutation