Intro to Immunology (Week 2 Lecture 3) Flashcards

1
Q

When did immunity first start being studied?

A

study began in the late 18th century with small pox outbreak (‘protection from diseases’)

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2
Q

What is immunity?

A

host’s defense against destructive forces from outside and within the body
* A versatile and coordinated defense system.
* Recognition (of something foreign) and Response (attack back)

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3
Q

Role of the immune system

A
  • Defense against infection.
  • Defense against tumors (can induce their own immune response)
  • Recognition of newly introduced molecules (proteins, transplants).
  • Source of inflammation (part of healing, inflammatory disease or autoimmunity).
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4
Q

What are the two immune responses?

A
  • innate
  • acquired
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5
Q

innate immune response

A

First immune response from birth which doesnt need to what the invading thing is to work effectively
* First response
* Immediate response
* Short term
* Non-specific (viruses, bacteria, etc.)
* Directs and initiates adaptive response

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6
Q

Acquired (adaptive) immune response

A

Aquiring the immunity is based on the characterisitics of what the infection is
* Second response
* Delayed response (days)
* Long term
* Requires exposure
* Has memory
* Specific and selective

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7
Q

Types of innate immunity

A
  • anatomic barriers
  • physiological barriers
  • eating cells
  • other cells
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8
Q

anatomical barriers

A
  • Skin
  • Mucous membranes
  • GI and respiratory tract (eat and breath in many toxins)
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9
Q

physiological barriers

A
  • Fever (growth inhibition)
  • Low pH (Stomach)
  • Chemical mediators
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10
Q

Eating cells

A

Phagocytes/ Endocytes are recruited to sites of infection where they recognize foreign molecule and ingest it (intracellular killing)
* Monocytes/Macrophages
* Neutrophils.

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11
Q

other cells (innate)

A
  • Dendritic cells, mast cells: Recruited to sites of infection, recognize and engulf
  • Natural Killers: surveillance/ killing/ transformed “self” cells (important for tumour surveillance to recognize self cells that have mutated)
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12
Q

Types of adaptive immunity

A
  • cell mediated immunity
  • humoral immunity
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13
Q

cell mediated immunity

A

Uses T-cells which are a type of white blood cell called lymphocytes. They help your immune system fight germs and protect you from disease.
* CD4 helper cells
* CD8 cytotoxic cells

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14
Q

CD4 helper cells

A

Help coordinate the immune response by stimulating other immune cells, such as macrophages, B lymphocytes (B cells), and CD8 T lymphocytes (CD8 cells), to fight infection.
* 5 subsets of CD4 cells (Th1, Th2, Th17, Treg and Tfh)
* IL-2, IFN- g cytokines (messengers between cells)
* targets intracellular bacteria

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15
Q

CD8 cytotoxic killer cells

A

Can directly kill cells harbouring pathogens, such as viruses
* TC1/ TC2 cells
* IL-4, IL-5, IL-10 cytokines (messengers between cells)
* extracellular bacteria antibody production

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16
Q

humoral immunity

A

Produces B cells which make antibodies to eliminate/ neutralize microbes outside the normal cell
* deals with antigens from pathogens that are freely circulating, or outside the infected cells.

17
Q

Organs involved in the immune system

A
  • Bone marrow: Origin and development (hence B cells)
  • Thymus and Spleen, GI tract: Education and selection
  • Lymph nodes: Reservoirs, circulation and traps
  • Lymphatic vessels, blood vessels: transportation
18
Q

Effect of nutrition on the immune system

A

One of the most sensitive systems in the body to changes in nutritional status
* measures of immune function are used to assess nutritional status

19
Q

What is the leading cause of immunodeficiency worldwide?

A

protein energy malnutrition

20
Q

futile cycle of immunity and poor nutrition

A
21
Q

Continuum of Immune Responses

A

need a balance of:
* cytokines: innate (IL-2, IFN- g) and adaptive (IL-4, IL-5, IL-10)
* eicosanoids, oxylipids
* hormones (corticosteroids/stress)
* other mediators

22
Q

The good of inflammation

A

Inflammation is essential for normal defense against pathogens and repair of tissue damage
* Redness, heat, swelling and pain
* Keeps us alive
* Means immune system is working effectively

23
Q

The bad of inflammation

A

sustained inflammation disrupts metabolic pathways and suppresses immune response:
* Excessive tissue damage
* Induce insulin resistance by disrupting insulin signalling
* Impair ability to defend against future infection

24
Q

Acute inflammation

A

Healing of tissue
* Immediate defense to tissue damage/injury
* Usually < 3 wks
* Neutrophils recruited to site
* Variable systemic effects
* Not necessarily associated with tissue destruction
* Followed by healing and repair
* Inflammation resolves

25
Q

Chronic inflammation

A

Low grade inflammation is constantly on and production can be disruptive systemically
* Excessive activation and/or insufficiently regulated immune system
* Sustained duration
* Macrophages, T-lymphocytes & their mediators predominate
* Significant tissue damage
* Systemic effects

26
Q

Commonly Measured Mediators

A
  • Glucocorticoid (stress hormones)
  • Interleukin-6 (IL-6)
  • Tumor Necrosis Factor (TNF-α)
  • Interleukin-1 (IL-1)
  • Interleukin-8 (IL-8)
  • Eicosanoids (prostaglandins)

Bolded are pro inflammatory

27
Q

Metabolic changes with chronic inflammation (tumor)

A
  • Liver (center of metabolism): ↑ Acute phase, ↓drug metabolism
  • Muscle: ↑ proteolysis, ↓ synthesis
  • Hypothalamus: ↓ appetite, ↑ sympathetic activity, ↑ REE, ↑ cortisol, ↓ testosterone
  • Gut: early satiety
  • produces C-reactive protein (non-specific)
  • Fat: ↑ lipolysis, ↓lipoprotein lipase
  • Brain: depression