Invertebrate Immunity Flashcards Preview

Introduction To Functional Marine Biology > Invertebrate Immunity > Flashcards

Flashcards in Invertebrate Immunity Deck (52)
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1
Q

What are the two types of immunity?

A

Innate immunity and acquired immunity.

2
Q

What is innate immunity?

A

The main defensive mechanisms found in invertebrates. It is naturally present and not due to prior sensitisation to an antigen from a infection or vaccination. It is nonspecific.

3
Q

What is acquired immunity?

A

Immunity that develops with exposure to various antigens.

4
Q

What are the three attributes of an immune system?

A

Reconnaissance, Recognition and Response.

5
Q

What is the first layer of immune defence?

A

The skin, which blocks most pathogens.

6
Q

What is the second layer of immune defense?

A

Physiological, where conditions such as temperature make the bodily environment more hostile for pathogens, e.g. stomach acid. Bivalves can rapidly change the pH of their mantle fluid, which pathogens cannot deal with.

7
Q

What is the third layer of immune defence?

A

The innate immune system, consisting of roaming scavenger cells such as phagocytes which engulf pathogens and debris. Phagocytes are only able to self & non self. Motivated strongly by metabolism.

8
Q

What is diapedesis?

A

When phagocytes migrate to an outer layer of the body and ‘spit out’ debris, so it is eliminated from the organism.

9
Q

What is the fourth layer of immune defences?

A

The adaptive immune system, which consists of cells called lymphocytes that adapt to the structure of pathogens to eliminate them efficiently.

10
Q

Why is the adaptive immune system called adaptive?

A

Because antibody shapes are tailored to the 3D shapes of different pathogens.

11
Q

When did the first T and B cells appear?

A

In the placoderms.

12
Q

What is the immune systems of the Porifera like?

A

They have carbohydrate–based self–recognition and can aggregate their own cells, organising them through intercellular signalling, eventually binding them together using proteins such as fibronectin. Capable of reacting to non–self material & enhanced allogenic rejection.

13
Q

How do Porifera react to non–self material?

A

They can deactivate non–self material by initiating melanin synthesis and using exopinacocytes and mesohyl (granule–bearing) cell types for endocytosis and lysozome release.

14
Q

What is melanin synthesis?

A

A defence system used throughout the invertebrates. Melanin is a disinfectant and when pathogens are coated they can be disinfected and in sufficient concentrations can even kill them.

15
Q

What is the immune systems of the Coelenterata like?

A

They show self and non–self recognition, complex cell signalling and phagocytic activity, as demonstrated by would healing. They produce non–specific antimicrobials e.g. oxygen radicals & antifungal(chitinase)/bacterial extracellular enzymes.

16
Q

How do the Coelenterata deal with non–self material?

A

Some gorgonians can isolate/inactivate foreign material by melanisation (black spots), & chitinase as most fungi have chitin in cell walls.

17
Q

What are oxygen radicals?

A

Powerful nonspecific disinfecting agents. Oxygen radicals are disruptive, and disrupts biological molecules. They are formed from peroxidase activity.

18
Q

What is the immune system of the Annelids like?

A

They have developed cellular immunity against pathogens, including phagocytosis, encapsulation and spontaneous cytotoxicity of coelomocytes against allogenic or xenogenic cells. They also have humoral immunity that is based on antimicrobial, haemolytic and clotting properties of their body fluids.

19
Q

What is encapsulation?

A

Circulating phagocytes surround and isolate the foreign material if unable to enzymically destroy it.

20
Q

What is humoral immunity?

A

Immunity based in body fluids.

21
Q

What is the immune system of the Mollusca like?

A

They have well developed self & nonself recognition that can be locally suppressed in brooding bivalves. They can produce lectins to bind to nonself material, preparing it for phagocytosis. Humoral antiviral activity has been found in some spp, and there is nonspecific antimicrobial superoxide activity.

22
Q

What are lectins?

A

They are proteins that bind to pathogens and fix them in lace & stimulate their phagocytic response.

23
Q

What is B–hyalinocyte?

A

It contains lots of endoplasmic reticulum, which produce metabolic enzymes which produce superoxides & get a respiratory burst. They secrete huge amounts of hydrogen peroxide & bring in phagocytes bc of messenger molecules in debris of pathogen & hyalinocytes.

24
Q

What is the immune system of the Arthropoda like?

A

They have a well developed innate humoral antiviral and antibacterial agents, wound repair systems that make use of exoskeletal formation systems and toll–like receptors for pathogen recognition. Some crustaceans have primitive immunological memory, with enhanced antibacterial response on second exposure and strain specific immunity passed to offspring in Daphnia magna.

25
Q

What are toll like receptors?

A

Proteins that are specific mostly to pathogens. They are used to recognise self and nonself via PAMP.

26
Q

What are PAMPS?

A

Pathogen Associated Molecular Patterns.

27
Q

What uses does the Limulus haemolymph have in human medicine?

A

It exhibits an extreme agglutination reaction when exposed to bacteria or even minute traces of bacterial endotoxins. It is therefore used to test the purity of intravenous saline & other medical media.

28
Q

What is LAL?

A

Limulus amoebocyte lysate.

29
Q

Why does Limulus haemolymph agglutinate when exposed to bacteria?

A

The agglutination is produced by the degranulation of amoebocytes.

30
Q

What are the immune systems of the Echinodermata like?

A

They have a well developed innate immune system that includes complement proteins analogous to the C3 proteins in vertebrates. There is also some evidence of an immunological memory (enhanced allogenic rejection) similar to acquired vertebrate immunological memory.

31
Q

What are the immune systems of the Chordata like?

A

Studies of tunicates shows well-developed self & non-self recognition, e.g. in colonial ascidians adjacent clone colonies will fuse but non-related colonies will produce lesions where they meet. They have non-specific TLRs and a variety of antibacterial peptides and a prophenoloxidase cascade wound response.

32
Q

What is a prophenoloxidase cascade wound response?

A

It’s activated when different receptors recognise PAMPs, which causes serine proteases to hydrolyze and activate proPAPs to PAPs. The PAPs then hydrolyze PPO, releasing PO. PO then oxidises tyrosine to DOPA, and then into quinones, which are the precursors to melanin, cytotoxic products and then encapsulation of pathogens.

33
Q

What are proPAPs?

A

Prophenoloxidase-activating proteinase precursors.

34
Q

What is PAP?

A

Prophenoloxidase-activating proteinase.

35
Q

What is PPO?

A

Prophenoloxidase.

36
Q

What is PO?

A

Phenoloxidase.

37
Q

What is DOPA?

A

Dihydroxyphenylalanine.

38
Q

What are T & B Cells?

A

The cellular components of vertebrate immune systems that recognise pathogens by the shape of molecules (antigens) on their surfaces. Vertebrate immune systems can produce a T & B-cell to fit every possible shape.

39
Q

What happens to T & B cells with the ability to bind to the body’s own cells?

A

They are destroyed, because if they were left in the body the result would be autoimmune disease.

40
Q

What does a B-cell do?

A

It attacks invaders outside cells.

41
Q

What do T-cells do?

A

They attack invaders inside cells.

42
Q

What are the functions of T-cells?

A

Having recognised non-self material, they have different jobs. Some send cytokines (chemical instructions) to the rest of the immune system, activating the appropriate defence systems. Others recognise and kill infected cells directly. Some help B-cells to make antibodies.

43
Q

What are the functions of B-cells?

A

With the help of T-cells, they produce antibodies that bind to antigens on the surface of pathogens, initiating the process of inflammation, firstly immobilising the pathogens by agglutination, then stimulating phagocytic macrophages and natural killer cells to engulf and digest the antibody-marked pathogens.

44
Q

What are the two regions of an antibody?

A

Variable and constant regions. The antibody is Y-shaped, with the arms being variable and the tail being constant.

45
Q

What does the variable region of the antibody do?

A

It provides specific binding of of pathogen epitopes.

46
Q

What does the constant region of the antibody do?

A

It defines the isotype that binds to other immune system components, e.g. macrophages.

47
Q

How are pathogens detected in the vertebrate immune system?

A

Detection is a consequence of binding between complementary chemical receptors. The surface of a lymphocyte is covered in receptors, and some pathogens will have epitopes with a high affinity for receptors,allowing them to bind and be detected.

48
Q

How is receptor diversity generated?

A

“Random” recombination of gene segments generates a combinatorial number of receptor varieties.

49
Q

What is affinity maturation?

A

The selection of effective receptors. Activated B-cells proliferate, producing mutated clones, which are selected by their affinity. High affinity clones are selected to form plasma cells and produce antibodies, or become memory cells. Low affinity clones cannot bind and undergo cell death.

50
Q

What effect does immune memory have on responses to pathogens?

A

Primary responses to new pathogens take an order of weeks, whereas memory of previously seen pathogens allows the secondary response to be in a matter of days with a much larger reaction.

51
Q

How are intra-cellular pathogens destroyed?

A

Tk-cells are activated by binding to a MHC/peptide complex on a self cell and costimulated by the innate immune system will destroy the self cell that presented the MHC/peptide complex.

52
Q

What is the role of the prophenoloxidase cascade in crustaceans?

A

Responds to pathogens and tissue damage by encapsulating and melanising pathogen and/or damaged tissues.