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Immunology and inflammation > IIM10: Paracites, hypersensitivity and allergy > Flashcards

IIM10: Paracites, hypersensitivity and allergy Flashcards

1
Q

What is a parasite defined as?

A

An organism that lives in or on a host organism at the expense of this host, eukaryotic organisms that cause infections

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2
Q

Give three examples of parasites

A

unicellular protozoa or multicellular helminths or arthropods

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3
Q

What are protozoa?

A

single-celled eukaryotes that can be divided into intracellular and extracellular pathogens

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4
Q

What is the problem with treating protozoa infections in humans?

A

There is limited immunological memory of protozoal infection, but no existing vaccines. Drugs against protozoa are also toxic to the host.

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5
Q

What group of parasite is malaria?

A

Protozoa

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6
Q

What has the biggest disease burden of all parasitic infections?

A

Malaria: 5 species of Plasmodium

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7
Q

How is malaria spread? Where is it most prevalent?

A

The protozoa are transmitted through mosquito bites from the female Anopheles mosquitoes and is prevalent in the tropics

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8
Q

Where are Plasmodium falciparum and Plasmodium vivax more prevalent? (each)

A

Plasmodium falciparum is prevalent in Africa whilst Plasmodium vivax is prevalent in Asia and South America.

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9
Q

What are the three stages of a plasmodium lifecycle?

A
  • > Sporozoites
  • > Merozoites
  • > Gametocytes
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10
Q

Explain the Sporozoites part of protozoa’s life-cycle

A

Released from the Anopheles mosquito into human blood

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11
Q

Explain the Merozoites part of protozoa’s life-cycle

A

Sporozoites infect liver cells, form a multinucleated mega cell known as a schizont which matures into merozoites that are released into the blood. These undergo proliferation in the RBCs and cause reinfection when RBCs rupture.

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12
Q

Explain the Gametocytes part of protozoa’s life-cycle

A

Merozoites can differentiate into male and female gametocytes which are ingested by an Anopheles mosquito, where they go through the sexual phase in the stomach of the mosquito to form sporozoites.

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13
Q

Where can most intracellular protozoa survive?

A

Within phagolysosomes

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14
Q

Where do merozoites that escape the liver cells remain?

A

In cellular vesicles

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15
Q

Why can merozoites that travel in cellular vesicles, reach distant parts of the circulation?

A

Cellular vesicles lack immunogenic features, thus remaining undetected

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16
Q

How do plasmodium take advantage of the humoral response?

A

They have been found to proliferate better in the presence of complement and antibody

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17
Q

How does protozoa hiding in RBC allow them to evade detection?

A

RBCs lack nuclei and cannot activate transcription in response to PRR activation.

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18
Q

If protozoa can evade detection via RBC then how does the immune system become activated?

A

Rupturing RBCs act as DAMPs which activate immune responses.

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19
Q

In the liver stage, RNA from the parasites growing in hepatocytes can be recognised by what?

A

MDA5

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20
Q

What does MDA5 activate?

A

MAVS-TBK1-IRF3/7 signalling that produces Type I IFNs.

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21
Q

In the blood stage, an APC ingests the parasites:

RNA is recognised by what?

A

TLR7

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22
Q

What is parasitic DNA is recognised by in the blood stage?

A

TLR9

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23
Q

What is parasitic GPI recognised by in the blood stage?

A

TLR2/1

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24
Q

What does TLR2/1 activate after recognising parasitic GPI?

A

MAPK and NF-kB signalling
MAVS-TBK1-IRF3/7 signalling
cGAS-STING-TBK1-IRF3 signalling

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25
Q

What does: MAPK and NF-kB signalling, MAVS-TBK1-IRF3/7 signalling and cGAS-STING-TBK1-IRF3 signalling produce?

A

Type I IFNs and proinflammatory cytokines

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26
Q

What do Schizont bursts release?
What are these sensed by?
What do they activate?

A

Haemozoin and uric acid which are DAMPs sensed by NLRP3 that also stimulates proinflammatory cytokine release

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27
Q

What type of protozoa is African sleeping sickness?

A

Extracellular

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28
Q

What is the name of the protozoa that cause trypanosomiasis (African sleeping sickness)?

A

Trypanosoma brucei

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29
Q

What is trypanosomiasis transmitted by?

A

Tsetse fly: T. brucei travels from the bite site into the blood via the lymphatics. From the blood, it can cross into tissues and even the brain.

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30
Q

Why was trypanosomiasis named sleeping sickness?

A

due to the effects of T. brucei in the central nervous system. The parasite stimulates inflammation and tryptophol release. Tryptophol is a compound that can induce a comatose state in the patient.

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31
Q

Where does T. brucei survive?

A

In the blood

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32
Q

How does T.brucei survive in the blood, despite humoral and cellular immune system components?

A

Through antigenic variation

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33
Q

How can T.brucei change its surface proteins?

A

by activating different variant-surface glycoprotein (VSG) genes at any time.

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34
Q

How many VSG genes does T.brucei posses?

A

roughly 1000

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35
Q

What does T.brucei’s possession of 1000 VSG genes mean it is able to do? What does this do to the human immune system?

A

Allows the parasite to repeatedly change its VSG and escape the humoral antibodies produced against a previous glycoprotein antigen. This causes a polyclonal IgM response that overshadows any effective adaptive immune response.

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36
Q

How do T.brucei prevent lysis by the alternative complement pathway?

A

The VSG is rapidly shed when an antibody or complement protein is encountered, preventing lysis by the alternative complement pathway, as not enough complement can be deposited to kill the cell.

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37
Q

Give another reason wy it is harder for the immune system to detect protozoa?

A

They are also eukaryotic cells, meaning that there are less PAMPs which separate our cells from theirs, making it harder for the innate immune system to detect them.

38
Q

What are Helminths?

Give three examples

A

multicellular eukaryotes which are generally known as worms; and include trematodes (flukes), cestodes (tapeworms), and nematodes (hookworm, pinworm, whipworm)

39
Q

What are the three stages in the life cycle of Helminths?

A
  1. Egg
  2. Larva
  3. Adult stage worm
40
Q

How can a host be invaded by Helminths?

A

skin penetration, ingestion of contaminated food or via insect vectors.

41
Q

Why can helminths not be phagocytosed and so opsonisation isn’t effective?

A

They are multicellular

- Complement could kill one cell at a time, but helminths have evolved defences against this.

42
Q

What are the primary immune defences against helminths?

A
  • Releasing toxins
  • Physically disturbing the infected area to eject the helminth – coughing, sneezing, itching, vomiting, diarrhoea or mucus.
43
Q

What presents parasite antigens to T helper cells?

A

Dendritic

44
Q

What do T helper cells differentiate into whenever they recognise parasite antigens on their cell surface?

A

TH2 cells that produce cytokines (IL-5 and IL-4)

45
Q

What are the cytokines that TH2 cells produce?

A

IL-5 – proliferation of eosinophils

IL-4 – class-switching of B-cells to produce specific IgE

46
Q

What can ILEs do?

A

They can opsonise the parasite; they are bound by the Fc receptors on mast cells and basophils which degranulate causing itches and muscle spasms to dislodge the parasite.

47
Q

Prolonged response to the parasite can lead to “walling-off” the parasite, how?

A

fibrosis

48
Q

What are the main effector cells against Helminths?

A

Granulocytes:

  • Mast cells
  • Basophils
  • Eosinophils
49
Q

Briefly describe the role of:

  • Mast cells
  • Basophils
  • Eosinophils
A

Mast cells – tissue-resident cells which degranulate upon activation through complement or IgE Fc binding and plays a key role in combating parasitic infections, allergy and anaphylaxis. In the absence of disease, the IgE concentration in the serum is the lowest of the five immunoglobulin subtypes.
Basophils – IgE-responsive cells which degranulate and can act as APCs.
Eosinophils – motile phagocytic cells which release eosinophil cationic protein and peroxidase which are key in responding to helminth infections.

50
Q

What is IgE production is reserved for?

A

Responses to large multicellular antigenic stimuli such as helminths

51
Q

When may IgE responses be inappropriate?

What does this mean helminths can trigger?

A

Exaggerated or by misdirecting the response to harmless antigens (e.g. pollen grains.)
Type I hypersensitivity reactions

52
Q

If the body fails to purge the parasite, what can result?

A

A granuloma will be formed (made of tightly packed macrophages) can be formed surrounded by a cage of ECM proteins produced through fibrosis. If the parasite remains unremoved, macrophages continue their inflammatory signalling and the immunopathology persists.

53
Q

What is Schistosoma?

A

A trematode that is transmitted to vertebrates from fresh-water molluscs.

54
Q

How do Schistosoma enter and colonise vertebrates?

A

Their larvae enter the blood stream from the skin or GI tract, and goes on to enter the organ in which it can sexually reproduce and produces eggs.

55
Q

How do Schistosoma damage humans?

A

Schistosomiasis’ most severe pathology is the immune response to the Schistosoma eggs, which it lays hundreds of daily. This causes tissue damage in the gut or bladder when exiting the body, or tissue disease in the liver caused by fibrosis and granulomas.

56
Q

What are chronic parasitic infections?

A

persistent parasitic burden or persistent symptoms

57
Q

If the parasitic burden is high but the pathology is low, this is called the ______ phenotype

A

tolerant

58
Q

What is characteristic of the tolerant phenotype?

A

Large amounts of TGF-b and IL-10 to activate Treg cells and produce IgG4 antibodies

59
Q

What allows the parasite to survive in the host with minimal collateral damage

A

Parasite antigens suppress parasite-specific T cell proliferation which reduces TH1 and TH2 cytokine levels

60
Q

If the parasite burden is low, but the pathology is high, this is called the _______ pathology and most adult parasites are killed

A

Chronic

61
Q

In chronic pathology which cytokines are at high levels?

A

IgE, TH1, TH2 and TH17 cytokines

62
Q

What do high levels of IgE, TH1, TH2 and TH17 cytokines cause?

A

severe inflammation as well as fibrosis and granuloma formation. This presents with Type I hypersensitivity due to chronic immune stimulation

63
Q

What advantage can chronic inflammation confer to the host? What does this mean?

A

concomitant immunity whereby being infected with a chronic malaria or Schistosoma infection prevents new infection from other parasite species.

64
Q

What is hypersensitivity?

A

an exaggerated immune response to a foreign substance which causes damage to host cells.

65
Q

What are the 4 types of hypersensitivity?

A

Type I – ‘A’llergic, ‘A’naphylaxis, ‘A’topy
Type II – anti’B’ody
Type III – immune ‘C’omplex
Type IV – ‘D’elayed

66
Q

Describe Type I hypersensitivity

A

It is triggered by an antigen which causes the crosslinking of IgE bound to Fc receptors on mast cells or basophils. This causes IgE-dependent degranulation which causes allergic symptoms such as hay fever or asthma.

67
Q

Describe Type II hypersensitivity

A

It is triggered by IgM or IgG inappropriately opsonising host protein antigens which activates the classical complement pathway and drives Antibody-dependent complement lysis of cells (ADCC). This can be seen when self-reactive antibodies are produced during rheumatic fever following streptococcal throat infections.

68
Q

Describe Type III hypersensitivity

A

It is triggered by the accumulation of immune complexes on cell surfaces when they are improperly cleared by macrophages. These trigger complement activation and the release of anaphylotoxins to induce neutrophil-mediated inflammation which causes tissue damage. This is especially seen with soluble antigens in the blood.

69
Q

Describe Type IIII hypersensitivity

A

It is triggered by an antigen activated pro-inflammatory TH1 cells which activate macrophages and cytotoxic CD8+ T cells which cause direct cellular damage. The delay in the response is due to the few days required to activate the cellular components. This reaction does not involve antibodies and is dependent of TH1 memory cells. Examples are food intolerance and skin reactions.

70
Q

What cytokines do T helper cells 1 produce?

macrophage, NK cell, T-cell

A 
(Group A)
IFN-y
TNF-a
IL6
IL-12
71
Q

What cytokines do T helper cells 2 produce?

mast cell basophill, T-cell

A

(Group B)
IL-4
IL-5
IL-10

72
Q

Based on the immune process that triggers each hypersensitivity, match the hypersensitivity types to the sort of infection would trigger normal versions of these responses?
Type 1-4
a) Protozoa parasites, bacteria, cells from other organisms
b) Viruses or other intracellular pathogens
c) Small repetitive antigens
d) Helminths

A

Type I: Helminths
Type II: Protozoa parasites, bacteria, cells from other organisms
Type III: Small repetitive antigens
Type IV: Viruses or other intracellular pathogens

73
Q

(basically) what does histamine cause?

A

irritation
itch
spasm

74
Q

Define atopy

A

The launching of an IgE response against inappropriate targets

75
Q

What are three major atopic diseases?

A

Allergy
Eczema
Asthma

76
Q

What does allergy describe?

A

a typically rapid acute response to diverse environmental antigens recognised by IgE (allergens). the response typically involves itching and swelling of the area that the allergen comes into contact with, as a result of IgE-triggered degranulation of mast cells and basophils.

77
Q

Give examples of allergies

A

hay fever (pollen allergies), food allergies, and insect bite allergies, and is sometimes used to include all atopic diseases.

78
Q

What can severe systemic (ie body-wide) allergic responses result in?

A

anaphylaxis

79
Q

What is anaphylaxis?

A

a rapid response to the allergen - typically an ingested food protein or insect bite venom - that has become distributed around the body. It can result in widespread vasodilation and fluid leakage (swelling) that can compromise the function of internal organs. In particular, anaphylactic responses in the heart or lungs can lead rapidly to death.

80
Q

What is the difference between food allergy and food intolerance?

A

Food intolerance is usually a result of enzyme deficiencies that compromise digestion, and usually has gastro-intestinal symptoms.

81
Q

What is another word for eczema?

A

Atopic dermatitis

82
Q

What is eczema?

A

an inflammatory skin condition characterised by itchy, damaged skin

83
Q

How can eczema be worsened?

A

frequent washing or scratching, and leaves the skin vulnerable to bacterial/fungal infection

84
Q

Where is eczema commonly found?

A

alongside other types of food intolerance or allergy. Conversely, eczema can often resolve spontaneously (eg as a child ages), presumably as the individual develops tolerance for the offending antigen

85
Q

What is asthma?

A

chronic inflammatory response to an antigen within the lungs. It is generally characterised by tightening or spasm of airways that results in difficulty exhaling.

86
Q

While the patient is generally well, certain exposures can trigger an _________ (asthma attack)

A

exacerbation

87
Q

What % of asthma sufferers do not respond to normal treatment?

A

10-30%

88
Q

What is most asthma caused by?

A

Ig-E induced

89
Q

What can asthma exacerbations be triggered by?

A

exercise, pollutants, even medication, alcohol, infections

90
Q

What treatment is provided to asthma sufferers

A

Broncho-dilating drugs or immune-suppressive steroids

91
Q

What is the hygiene hypothesis?

A

There are higher levels of atopic disease where people grow up in more sterile environments. In particular this seems to be associated with reduced exposure to helminths or arthropod parasites: allergy is rare in Africa (where there is a large parasite burden), and much more common in developed nations, particularly urban areas, and less common in people with pets. The hypothesis is that if our immune system is not exposed to pathogens that stimulate IgE responses, then our immune system will be more highly sensitised to react to something else - such as an innocuous allergen.

92
Q

What are the suggestions for how atopic diseases arise?

A

it is possible that molecular mimicry mechanisms can induce atopic diseases
Genetic
Environmental factors: some chemical exposure can promote development of various intolerances, while exposure to a suitable antigen is necessary

Immunology and inflammation (11 decks)

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