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SEM 4: Immunology > Review of The Innate Immune System > Flashcards

Review of The Innate Immune System Flashcards

1
Q

Why do we need the innate immune system?

A

The adaptive immune response (antibodies etc) takes too long so we need the innate immune system to allow us to survive long enough for the specific response.

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2
Q

Which organisms have adaptive immunity?

A

Vertebrates have adaptive immunity whereas invertebrates are able to survive with just the innate response.

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3
Q

What is adaptive immunity?

A

Adaptive immunity is a specific response to infection involving specific recognition of infectious agents i.e. antigens.

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4
Q

What is innate immunity?

A

Recognition of broadly conserved features of different classes of pathogens to protect us e.g. structure of ell walls, staining and binding activity etc.

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5
Q

What does innate immunity consist of?

A

Consists of:

  • Phagocytosis
  • The inflammatory response
  • Cytokines, interferons and anti-microbial peptides (AMPs)
  • Complement
  • Intrinsic defences - “the hostile cell”
  • NK cells
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6
Q

What is phagocytosis?

A

The ability of specialised cells to recognise something as “foreign” and digest it.

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7
Q

Give an example of a phagocytic cell in the horseshoe crab

A

Amoebocyte

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8
Q

Which cells carry out phagocytosis in vertebrates?

A

Dendritic cells
Macrophages
Neutrophils
These are NOT the same cell.

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9
Q

What is the action of dendritic cells in phagocytosis?

A
  1. Detect a pathogen
  2. Engulf the pathogen
  3. Stop any further phagocytosis
  4. Traffic to the lymph nodes and break down the pathogen
  5. Present the pathogen peptides to MHC class II and educate the adaptive immune system
  6. Leads to stimulation of the division of naive T and B cells
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10
Q

What is the action of macrophages in phagocytosis?

A
  1. Act as a tissue resident and present antigens.
  2. They do not trigger the immune response but activate memory.
  3. Involved in cleaning and repairing damage
  4. Go into tissue during an infection
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11
Q

What is the action of neutrophils in phagocytosis?

A

Rarely tissue resident
1. Circulating in the body
2. When infection is triggered, they are recruited to the site of infecton and inflammation.
3. Increase the no. of neutrophils and these cells do most of the phagocytosis.
4. Do not care what they destroy however so can cause a lot of tissue damage.
Chronic inflammation can cause of lot of diseases and is associated with a high number of neutrophils.

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12
Q

What is the purpose of phagocytosis?

A

Clears pathogens but also present peptides on MHCs which promotes development reactivation of the adaptive immune response.

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13
Q

What are the two distinct roles of macrophages?

A
  1. Help phagocytosis
  2. Send information to ensure immune system works in a coordinated way by producing cytokines and chemokines to stimulate the innate and adaptive response. They do this by triggering the inflammatory response and promoting the local antmicrobial state.
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14
Q

What is the inflammatory response?

A

A generic defence mechanism whose purpose is to localise and eliminate injurious agents (stop pathogens leaving the site of infection) and to remove damaged tissue componenets (done by a specific type of macrophage).

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15
Q

What occurs during the inflammatory resposne?

A
  • Enhanced permeability of endothelial cells and extravasation
  • Neutrophil recruitment
  • Enhanced cell adhesion
  • Enhance clotting
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16
Q

What are cytokines and chemokines?

A

Both glycoprotein hormones that affect the immune response.

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17
Q

What do cytokines do?

A

Act as specific signals to modify the behaviour of cells in the immune response. Most of them are called interleukins (e.g. IL-1) however there are others such as interferon

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18
Q

What do chemokines do?

A

Act as chemotactic factors by creating concentration gradients which attract (or occasionally repel) specific cell types to the site of production/infection.

19
Q

What is the IL-1?

A

A major enhancer of the inflammatory response

20
Q

What is IL-8?

A

In macrophages and is normally regulated unless the macrophage is infected then acts as a chemoattractant for neutrophils.

21
Q

What is the role of TNF-alpha?

A

Important in opening up the endothelium and triggers antiviral response.

22
Q

How do phagocytes know what to digest?

A

Material to be eaten is recognised by:

  • Detection of phosphatidylserine on the exterior membrane surfaces as this is on cells that are apoptosis
  • By scavenger receptors
  • By some Toll-Like receptors which are pattern recognition receptors
  • By passive sampling
23
Q

What are pathogen-associated molecular patterns (PAMPs)?

A

They are molecules that are present only on pathogens and not on host cells and essential for their survival. They are invariant structures that are shared by entire classes of pathogens.

24
Q

What are the PAMPs for gram-negative bacteria?

A

Lipopolysaccharides (LPSs) found in outer membranes (also endotoxins)

25
Q

What are the PAMPs for gram-positive bacteria?

A

Teichoic acid, lipoteichoic acid, peptidoglycan found in outer membranes

26
Q

What are other examples of PAMPs?

A
  • Bacterial flagellin
  • Abnormal protein glycosylation - differs between higher, lower eukaryotes and prokaryotes
  • Abnormal nucleic acids such as in viruses which have differences between their nucleic acids and the hosts
27
Q

What are pattern recognition receptors (PRRs)?

A

They are host factors that specifically recognise a particular type of PAMP. They are germ-line encoded. They are categorised by function: either extracellular or intracellularly.

28
Q

What are extracellular PRRs?

A

Recognise PAMPs outside of the cell and trigger a coordinated response to the pathogen e.g. recognise bacteria that is around the outside of the cell.

29
Q

What are intracellular PRRs?

A

Recognise PAMPs inside a cell and act to coordinate a response to the pathogen i.e. all viruses are intracellular.

30
Q

What are secreted PRRs?

A

They are secreted and act to tag circulating pathogens for elimintation e.g. complement system.

31
Q

What is complement?

A
  • A heat-sensitive component of serum that could augment the ability of antibodies to inactivate antigens.
  • A biochemically complex antibody-dependent effector mechanism leading to: help antibodies recognise and kill pathogens.
32
Q

What is the complement system?

A
  1. Opsonisation: complement is recruited and forms a hard shell with complement proteins around the pathogen.
  2. The recruitment of phagocytic cells, vasoactive function involves the recruitment of complement to the surface to release phagocytes and increase vasoactivity.
  3. Then, holes are punched into target membranes (MAC) of the bacteria/pathogen.
    This is an adaptive immune function.
33
Q

What is the role of complement in the innate immune response?

A

They act as secreted PRRs and can be activated by a range of PAMPs as well as activated by “altered self”. It is an evolutionary system which predates the development of the adaptive response. The adaptive response is an adaption that formed later.

34
Q

What are the three complement pathways?

A
  1. Classical: antibodies pathway but also C1q that recognises LPS without antibodies. It recognises and allows opsonisation.
  2. Lectin: recognises abnormal glycosylation of proteins.
  3. Alternative: recognises any surface that is not the same as the host.
35
Q

What are interferons?

A

They are secreted glycoproteins/peptide factors (type I and type III) which are released in response to viral infection. They offer cross-protection (can be used against a lot of infections) and are widely distributed across evolution.

36
Q

What is the interferon system?

A
  1. Cell is infected by a virus
  2. Cell replicates and if there is no antiviral response the cell will apoptose and spread more of the virus.
  3. During primary infection, interferon is secreted and binds to neigbouring cells.
  4. An antiviral state is triggered in the neigbouring cells so when the virus tries to enter it is unable to.
37
Q

What is the anti-viral state produced by interferon?

A

It will set up a signalling transduction system and lots of genes are switched on. For example; protein kinase R which is upregulated by interferon and needs a cofactor which is double stranded RNA from viruses to PKRa which stops the production of the viral proteins. However, this is also bad for hosts as it stops all protein production.

38
Q

What are anti-microbial peptides (AMPs)?

A

They are short secreted peptides (18-45 amino acids long) that work by disrupting the cell wall leading to lysis as they insert pores. Some are induced by bacterial infection and they offer broad protection but not much is known about these.

39
Q

What is the “the hostile cell” concept?

A

The concept that cells have biochemical mechanisms that discourage viral replication such as apoptosis, restriction factors/intrinsic immunity, epigenetic silencing, RNA silencing and Autophagy/Xenophagy.

40
Q

Why do some viruses induce apoptosis and some not?

A

Some viruses such as the SeV virus in mice triggers apoptosis but the virus Ebola in humans does not. It is able to block apoptosis which is why it is a good pathogen as it is able to undermine apoptosis.

41
Q

What are natural killer cells?

A

Major component of the innate immune system for some viruses particulary herpes virus.
4% white blood cells. They are lymphocyte-like but larger with granular cytoplasm. They kill certain tumour and virally infected cells using a mechanism called loss-of-self.

42
Q

What causes targetted cell destruction in NK?

A

Cytotoxic molecules called granzymes and perforins.

43
Q

Describe the process of loss of self in NK cells

A
  1. Triggers recognition of pathogens by T cells by breaking down pathogen peptides and presenting them through MHC class I.
  2. In an uninfected cell, they will see that the pathogen is not on it, inhibitory signal, and will not kill it.
  3. Pathogens are able to remove MHC class I and cannot present peptides to the T cells.
  4. NK will recognise the absence of a signal and then inject perforins to induce cell death in an infected cell.
  5. NK can also recognise and lyse virally infected cells and certain tumour cells.
    Selectivity is conferred by loss of “self” MHC molecules on target cell surfaces, AND up-regulation of activating ligands.
44
Q

Compare and contrast innate and adaptive immunity

A

Innate:

  • macrophages, neutrophils, DCs
  • fast response
  • no memory cells
  • low specificity
  • pattern recognition receptors
  • has microbial ligands that are highly conserved between pathogens and germ-line encoded receptors evolved by natural selection.

Adaptive:

  • lymphocytes
  • slow response
  • memory cells
  • Ig and TCR receptors
  • Billions of possible antigens. Receptors generated randomly within individual; and cannot be inherited.

SEM 4: Immunology (15 decks)

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