CH 1: Intro to the Immune System Flashcards

1
Q

What is immunology?

A

Study of the physiological mechanisms that humans and other animals use to defend their bodies from invasion by pathogens
- study of the immune system

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2
Q

How does our body defend itself against pathogens?

A

immune system

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3
Q

3 broad categories of defense

A
  1. Physical & chemical barriers
  2. Innate response (born w/ it)
    - divided into immediate & induced
  3. Adaptive response
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4
Q

Pathogen

A

Any organism w/ the potential to cause disease
- can habitually cause disease or be opportunistic

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5
Q

Opportunistic

A
  • normally already in our body at normal levels…occurs when at high levels
  • will not always have the opportunity to cause disease
  • must have certain conditions met
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6
Q

What does it mean to be immune to infection?

A

Built up resistance to a disease/infection

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7
Q

How do we become immune?

A
  • natural selection
  • vaccines
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8
Q

Immunization (vaccination)

A

Procedure to prevent severe disease by prior exposure to the infectious agent in a form that cannot cause disease
- purposeful exposure
- adaptive response

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9
Q

Immunization: history

A
  • 1st used against smallpox in 18th century
  • Lady Mary Wortley Montagu
    —-small amounts of smallpox virus
  • Edward Jenner = cowpox
    —-similar to smallpox, but not deadly
    —-father of immunology
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10
Q

variolation

A

Make a cut in non-infected persona & expose them

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11
Q

Different forms of vaccines

A
  • mRNA
  • dead pathogens
  • can mutate virus, “killed off” vaccines
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12
Q

Commensal microorganism

A

Habitually lives on or in the human body; normally does not cause disease & can be beneficial
- can make vitamins, process digested food, and protect against disease
- 1000+ microorganisms live in healthy adult gut, adding 10 lbs body weight

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13
Q

Commensal microorganism pt 2

A
  • the reason why we lose lbs when given antibiotics…
  • microorganisms died, but will regrow
  • in gut, skin, etc
  • take up space INSTEAD of pathogens
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14
Q

Microbiota

A

Community of microbial species that inhabit a specific niche in the human body
- skin, mouth, gut, vagina

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15
Q

vaginal vs c-section

A

importance of early exposure to microorganisms

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16
Q

Colon

A

The colon is colonized by large numbers of commensal bacteria
- antibiotics kill many of these com. bacteria
- pathogenic bacteria gain a foothold & produce toxins that cause mucosal injury
- rbc & wbc leaks into gut between injured epithelial cells

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17
Q

Four types of pathogenic organisms

A
  • Viruses: intracellular (need a host)
  • Fungi: extracellular
  • Bacteria: extracellular
  • Parasites: extracellular
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18
Q

Defenses (extracellular)

A

scratching, diarrhea, vomitting

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19
Q

Barriers help keep what away?

A

pathogens

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20
Q

Relationships of pathogens and humans change over time

A

Most pathogenic organims evolved adaptations to allow them to invade the host, replicate in them and be transmitted
- “new” pathogens often cause high mortality (ebola)
- rapid death of host not good for pathogen

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21
Q

Human population in the evolution of pathogens

A
  • evolve a degree of built-in genetic resistance
  • acquire lifetime immunity to endemic diseases
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22
Q

endemic diseases

A

ubiquitous and people often exposed in childhood
- measles, chicken pox

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23
Q

Pathogens evolve to become..

A

Less pathogenic
- mortality bad for both humans & pathogens

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24
Q

Epithelium

A

Layers of cells that line the outer surface & inner cavities of the body
- strong barriers: skin, hair, & nails (provides chemical & physical barrier)
- more vulnerable: mucosal surfaces (mucosae)–secrete mucus, thick fluid that protects epithelial cells from damage and infection

25
All epithelia produce what?
Antimicrobial peptides - kill pathogens by perturbing their membranes
26
Tears & saliva
Secrete lysozyme that degrades bacterial cell walls - level of protection - ex : dust in your eyes
27
Stomach & vagina
Very acidic
28
If barriers are breached...
Innate immune response
29
Innate immune response
Born with; initiated immediately upon infection - non-specific, localized defense against wide range of pathogens - 2-part response
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Innate immune response: 2-part response
1. Recognition that a pathogen is present - soluble proteins & cell-surface receptors bind to the pathogen & its products or to altered human cells 2. Recruitment of effector mechanism - processes used to destroy & remove pathogens
31
Effector mechanisms
- Effector cells - Complement
32
Effector cells
Engulf bacteria, kills virus-infected cells, or attack parasites (macrophages, NK cells)
33
Complement
Serum proteins that mark pathogens in order to attack them or alter effector cells
34
Innate immunity
Host defense mechanisms that act at start of infection
35
Pathogen-recognition mechanisms
- Bacterial cell surface induces cleavage & activation of complement - One complement fragment covalently bonds to the bacterium, the other attracts an effector cell - The complement receptor on the effector cell binds to the complement fragment on the bacterium
36
Effector mechanisms
The effector cell engulfs the bacterium, kills it, and breaks it down
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Innate immunity (general process)
- Healthy skin is not inflamed - Surface wound introduces bacteria, which activate resident effector cells to secrete cytokines - Vasodilation & increased vascular permeability allow fluid, protein, and inflammatory cells to leave blood & enter tissue - The infected tissue becomes inflamed, causing redness, heat, swelling, & pain
38
Edema
Swelling
39
Cytokines
Soluble proteins secreted by cells to change behavior of surrounding cells - produced when cells detect infection; react w/ other cells to trigger innate immune response - make blood vessels leaky to allow fluids & other things to exit blood vessel & enter the infection
40
Inflammatory cells
WBCs present in inflamed tissues; contribute to inflammation
41
If infections outrun innate immune responses
Adaptive immune response
42
Adaptive immune response
Response of antigen-specific B and T lymphocytes to antigen - involves development of immunological memory - adapts to the infecting protein - highly specific (of the type of cell) - evolved only invertebrates
43
Lymphocytes
B, T, and NK WBCs - B & T are small - WBCs are large, also involved in innate response
44
Antigen
Molecule or molecular fragment recognized by an antibody or B or T cells - may also be proteins, toxins, etc
45
Recognition mechanisms: Innate vs Adaptive response
Innate: - rapid response (hrs) - fixed - limited number of specificities - constant during response Adaptive: - slow response (days to weeks) - variable - Numerous highly selective specificities - improve during response
46
Innate and Adaptive responses have common what?
Common effector mechanisms for the destruction of pathogens
47
Specificity of adaptive immune response
Lymphocyte receptors encoded by genes that are cut, spliced and modified during lymphocyte development. - clonal selection - clonal expansion
48
Clonal selection
Stimulation of a small subset of pathogen-specific lymphocytes for proliferation
49
Clonal expansion
Proliferation and differentiation of selected lymphocytes - large clones of antigen-specific lymphocytes generated to fight the infection
50
Adaptive immune response is faster/slower than innate immune response?
Slower!
51
Different receptors...
Different antigens
52
Memory cells
Lymphocytes selected during an adaptive immune response that persist after the infection - allow for immunological memory - subsequent infection by same pathogen elicits stronger and faster adaptive immune response
53
Acquired/protective immunity
Adaptive immunity provided by immunological memory
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Primary immune response
First encounter with pathogen
55
Secondary immune response
All subsequent encounters with that pathogen - anything after primary response, bc don't know how many times exposed
56
In order for adaptive response to be activated what happens first?
NEED innate response first
57
Vaccinations induce what?
Immunological memory - B & T cells memory - adaptive responses contingent upon innate responses...so vaccines must induce BOTH
58