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MD2002 Arvin > Innate Immunity COPY > Flashcards

Innate Immunity COPY Flashcards

1
Q

What is the body’s first line of defence against pathogens ?

A

Innate Immunity

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2
Q

Is innate immunity specific ?

A

No

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3
Q

Is adaptive immunity ?

A

Yes

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4
Q

Describe the route of entry, mode of transmission, and pathogen for the following diseases:

  • Influenza
  • Meningococcal Meningitis
  • Typhoid Fever
  • Diarrhea
  • Syphillis
A

INFLUENZA

  • Route: Airway
  • Transmission: Inhaled droplets
  • Pathogen: Influenza virus

MENINGOCOCCAL MENINGITIS

  • Route: Airway
  • Transmission: Inhaled droplets
  • Pathogen: Neisseria meningiditis

TYPHOID FEVER

  • Route: GI tract
  • Transmission: Contaminated food or water
  • Pathogen: Salmonella typhi

DIARRHEA

  • Route: GI tract
  • Transmission: Contaminated food or water
  • Pathogen: Rotavirus

SYPHILLIS

  • Route: Genito-urinary
  • Transmission: Physical contact
  • Pathogen: Treponoma pallidum
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5
Q

How may pathogens gain access ?

A

Through mucosal surfaces

Through external epithelia

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6
Q

Identify examples of diseases which involve pathogen access to mucosal surfaces.

A 
Influenza
Meningococcal meningitis
Typhoid fever
Diarrhea
Syphillis
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7
Q

Identify examples of diseases which involve pathogen access through external epithelia.

A 
Athlete’s foot
Anthrax 
Tetanus
Yellow fever 
Malaria 
Lyme disease
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8
Q

Describe the route of entry, mode of transmission, and pathogen for the following diseases:

Athlete’s foot
Anthrax 
Tetanus
Yellow fever 
Malaria 
Lyme disease
A

ATHLETE’S FOOT

  • Route: External surface
  • Transmission: Physical contact
  • Pathogen: Tinea Pedis

ANTHRAX

  • Route: Wounds and abrasions
  • Transmission: Minor skin abrasions
  • Pathogen: Bacillus anthracis

TETANUS

  • Route: Wounds and abrasions
  • Transmission: Punctures
  • Pathogen: Clostridium tetani

YELLOW FEVER

  • Route: Insect bites
  • Transmission: Moquito
  • Pathogen: Flavivirus

MALARIA

  • Route: Insect bites
  • Transmission: Moquito
  • Pathogen: Plasmodium

LYME DISEASE

  • Route: Insect bites
  • Transmission: Ticks
  • Pathogen: Borrelia burgdorferi
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9
Q

What are the three phases of response to initial infection ? Identify the onset/duration of each

A

1) Innate Immunity (0-4 hours)
2) Early induced response (4-96 hours)
3) Adaptive Immune Response (>96 hours)

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10
Q

What are the main steps in innate immunity (step 1 of response to initial infection) ?

A

Infection –> Recognition by preformed, nonspecific effectors –> Removal of infectious agent

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11
Q

What are the main steps in early induced response (step 2 of response to initial infection) ?

A

Infection –> Recruitment of effector cells –> Recognition and activation of effector cells –> Removal of infectious agent

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12
Q

What are the main steps in adaptive immune response (step 2 of response to initial infection) ?

A

Infection –> Transport of antigen to lymphoid organs –>

Recognition by naive B and T cells –> Clonal expansion of effector cells –> Removal of infectious agent

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13
Q

What are the main types of barriers to infection ?

A

Mechanical, chemical, microbiological

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14
Q

Give examples of mechanical barriers to infection.

A
  • Tight junctions between cells prevents access
  • Air and fluid flow across epithelium
  • Movement of mucus by cilia
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15
Q

Give examples of chemical barriers to infection.

A
  • Fatty acids on skin
  • Enzymes: lysozyme in saliva, sweat and tears.
  • Low pH in stomach
  • Antibacterial peptides: defensins (skin and gut) cryptidins (gut)
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16
Q

Give examples of microbiological barriers to infection.

A

-Normal flora compete for nutrients and attachment (biofilms), and also produce antibacterial substances (colicins)

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17
Q

What happens once a microorganism has gone across an epithelial barrier ?

A

Recognised and ingested by mononuclear phagocytes, or macrophages.

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18
Q

What are examples of receptors on phagocytes which aid recognition of microorganisms ?

A 
Mannose receptor 
Glucan receptor 
Scavenger receptor 
CD14  
CD11b/CD18
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19
Q

What are some of the bactericidal effects and agents produced by phagocytes ?

A
  • Acidification: pH 3-4, bactericidal
  • Toxic oxygen derived products: superoxide, hydrogen peroxide, hydroxyl radical
  • Toxic nitrogen oxides: Nitric Oxide
  • Peptides: defensins and other cationic proteins
  • Enzymes:Lysosyme, acidhydrolases
  • Competitors: Lactoferrin, vitamin B12 binding protein
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20
Q

What is the progenitor cell of all cellular elements of blood, rbc, platelets, white cells (including macrophages, T cells etc.) ?

A

Hematopoietic stem cell

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21
Q

What is a monocyte ? What is the difference between a monocyte and a macrophage ?

A

Monocytes: one of the three types of phagocytic cell of the immune system.
Circulate in bloodstream, differentiate into macrophages in tissue.

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22
Q

What is another name for granulocytes ?

A

Polymorphonuclear (PMN) leucocytes

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23
Q

What are the main types of granulocytes ?

A

Neutrophils, Eosinophils, Basophils

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24
Q

What are the main types of WBCs ?

A

Lymphocytes
Granulocytes (Neutrophils, Eosinophils, Basophils)
Monocytes (–> Macrophages)

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25
Q

What are the main phagocytic cells of the immune system ?

A

Neutrophils, Monocytes, Dendritic Cells

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26
Q

What is the most important/numerous cell of innate immunity ?

A

Neutrophils

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27
Q

What is the main function of eosinophils ?

A

Parasite defence

28
Q

What is the most common granulocyte/Polymorphonuclear leukocyte ?

A

Neutrophils (99% of all PMNs)

29
Q

What proportion of all leucocytes do neutrophils make up ?

A

70%

30
Q

How long do neutrophils survive in circulation, and in tissue ?

A

In circulation, around 12 hours, once in tissue survive for maybe only 2 days.

31
Q

How many rounds of phagocytosis can neutrophils usually undertake ?

A

Just one

32
Q

What are the main features of Chronic granulomatous disease ?

A

Failure in respiratory burst
Superoxide production limited
Sntibacterial activity impaired

33
Q

Why and how may neutrophils adapt ?

A

To prevent growth of parasites that can live in phagocytic cells.

34
Q

How is the short life span of neutrophils beneficial ?

A

Since antimicrobial products damage host tissues, short lifespan may limit host damage

35
Q

What are the consequences of Alpha 1-antitrypsin deficiency ?

A

Elastase from neutrophils not adequately inhibited, excessive tissue damage during inflammation (e.g. in pulmonary emphysema)

36
Q

What are the contents of the eosinophil granules ?

A

Histamine, peroxidase, RNase, DNases, lipase, plasminogen, Major Basic Protein

37
Q

How long do eosinophils survive in circulation, and in tissue ?

A

Circulate for 12 hours, survive in tissues for 3 days

38
Q

What is eosinophilia ? When might it occur ?

A

Increase in number of eosinophils, more than 500 per microlitre blood
May occur in parasitic infections of gut, some vascular diseases, Hodgkin’s Disease, Addison’s Disease

39
Q

What is eosinopenia ? When may it occur ?

A

Decrease in number of eosinophils

When glucocorticoids are used

40
Q

Describe the main features of Eosinophilia-myalgia syndrome (EMS).

A

Possibly fatal neurological condition
Eosinophils increased in blood
Potential interference with histamine metabolism

41
Q

What is the function of basophils ?

A

Similar and complementary to eosinophils and mast cells.

42
Q

What is the function of mast cells ?

A

When activated release a number of substances that effect vascular systems (e.g. due to IgE mediated triggering in allergies)

43
Q

Which is the least common Polymorphonuclear leukocyte ?

A

Basophils

44
Q

What are some of the substances secreted by basophils upon activation ?

A

Histamine
Proteoglycans
Leucotrienes
Some cytokines including IL-4 (potentially important for IgE and allergy)

45
Q

What are the types of lymphocytes ?

A

Beta or T lymphocytes

46
Q

What is the function of each of beta and T lymphocytes ?

A

B-cells produce antibody

T-cells becoming cytotoxic T cells (CD8) or helper T cells (CD4)

47
Q

What is the most important cell of the adaptive immune response ?

A

Lymphocytes

48
Q

What are plasma cells ? What is their role ?

A

Activated beta-cells

Makes large amounts of a specific antibody.

49
Q

Which kind of leukocyte are Natural Killer Cells ? What is their role ?

A

Large granular lymphocytes

Recognise virally infected cells non- specifically

50
Q

What is the main role of dendritic cells ?

A

Bridges innate and adaptive immune responses

Specialised in antigen uptake and antigen presentation

51
Q

What responses do viral-infected cells produce ?

A

Produce alpha and beta interferons which:

  1. Induce resistance to viral replication in all cells
  2. Increase MHC class 1 expression and antigen presentation in all cells
  3. Activate NK cells to kill virus-infected cells
52
Q

What is the key difference between NK cells and CD8 cells ?

A
  • NK cells are not antigen specific
  • NK cells do not require to undergo the lengthy clonal expansion of T cells in lymph nodes when virus is detected (hence quicker response)
53
Q

How quick is the NK response to viral infection ?

A

Quick (starts around day 2)

54
Q

How do NK cells know whether or not to kill a cell ?

A

Through interaction of its own surface activator receptor and inhibitory receptor with molecules on the surface of cells.
Inhibitory receptor of NK cell binds to MHC 1 protein so if MHC 1 present, negative signal predominates and killing does not take place (in healthy cell, still get positive signal because activating receptor of NK cell still interacts with a protein on healthy cell but negative signal predominates).

In a virus infected cell, MHC 1 expression is downregulated so inhibitory receptor has nothing to bind with whereas activating receptor does. i.e. positive signal predominates and NK cell kills virus infected cell.

55
Q

What kind of molecule if a complement ? What is its function ?

A

Heat labile component of plasma that act in concert with

antibodies to kill some bacteria

56
Q

What are the activation pathways which exist that trigger the complement cascade ?

A
  1. Classical Pathway: Antibody binds to specific antigen on pathogen surface
  2. Lectin Pathway: Mannose-binding protein binds to pathogen surface
  3. Alternative Pathway: Pathogen surface creates local environment conducive to complement activation
57
Q

What is the consequence of the complement activation (as a result of the classical, lectin, and alternative pathways) ?

A
  • Recruitment of inflammatory cells
  • Opsonisation of pathogens (facilitates uptake and killing by phagocytic cells)
  • Lysis and death of pathogens
58
Q

What is the function of C3b, C3a, C5a ?

A

C3b: opsonin
C3a: Peptide mediator of inflammation
C5a: Peptide mediator of inflammation

59
Q

What is the start and end point of the complement cascade ? How does it get from one to the other ?

A

C1 through C9 (cleavage of one into two again and again)

60
Q

How is the classical pathway initiated ?

A

By activation of C1 complex

61
Q

How is the lectin pathway initiated ?

A

By activation of a complex made of MBL MASP-1 and MASP2.

62
Q

How is the alternative pathway initiated ?

A

By spontaneous hydrolysis of serum C3

63
Q

What are some factors which increase phagocytosis ?

A

Antibody binding + Opsonisation

64
Q

What is the membrane attack complex (MAC) ?

A

Using complements C5 through C9, membrane attack complex forms.
This punches pores in surface of bacteria
Contents leak out
Lysis takes place

65
Q

How is the complement cascade system regulated ?

A

Through regulatory proteins such as:

  • Factor H (makes complement more susceptible to cleavage and inactivation by Factor I)
  • C1 inhibitor (dislodges interaction between C1r and C1s, and active C1 complex in the classical pathway)
  • CD59 = protectin (present in most cells in the body, to prevent final assembly of MCP in normal body cels)
66
Q

What are possible causes of neutropenia ?

A

Genetic or due to medication including chemotherapy

MD2002 Arvin (110 decks)

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