Animal Lesson 7 Flashcards

1
Q

Pathogen

A

Any foreign thing that’s not supposed to be there (virus, bacteria, etc).

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2
Q

Innate immunity

A

In all animals. Recognition of traits shared by broad ranges of pathogens, using a small set of receptors to recognize it. Rapid response as it happens as soon as you get infected. Includes Barrier and internal defences.

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3
Q

Adaptive immunity

A

Vertebrates only. Recognition of traits specific to
particular pathogens, using a vast array of receptors. Lock and key finds the actual pathogen and targets it one on one. Slower response. Third line of defence. Have humeral and cell-mediated response.

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4
Q

Vertebrates

A

Animals with a backbone (fishes and humans).

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5
Q

Barrier defenses

A

The first line defence (primary defence).
* Skin
* Mucous membranes (will trap things from getting in)
* Secretions

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6
Q

Internal defences

A

The second line of defence. If they break into the body. They will target everything in hopes of getting everything.
* Phagocytic cells
* Natural killer cells
* Antimicrobial proteins
* Inflammatory respons

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7
Q

Humoral response

A

Antibodies defend against infection in body fluids (blood, interstitial, lymph).

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8
Q

Cell-mediated response

A

Cytotoxic cells defend against infection in body cell (cells that have already been infected). They try to kill these infected cells.

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9
Q

Barrier defenses prevent what?

A

most pathogens from entering the body. We wash our hands to get rid of bacteria.

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10
Q

Skin/Shells/Cuticle (in worms)

A

Thickened outer surface inhibits entry by pathogens. It’s physical barrier.

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11
Q

Mucous membranes

A

Mucus (thicken fluid) secreted by internalized external surfaces (ie. nose, mouth, body parts that face the outside but are internal) traps microbes and other particles.

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12
Q

Secretions – saliva, tears

A

Washing action prevents microbial colonization (when they divide and divide). Hostile chemical environment: Lysozyme, acidic pH (that prevent the growth of pathogens).

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13
Q

Phagocytic Cells

A

Recognize molecules characteristic of a set of pathogens (not from own body) and will engulf it. That recognized molecule is absent from vertebrates
and is an essential component of certain groups of
pathogens. The molecule that its recognizing has to be one of the things that the virus needs to survive but can’t be found in our own bodies or else we will start eating our own cells.

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14
Q

Why is it important for the component to be essential
to the pathogen?

A

So they don’t adapt and evolve into something else that’s unrecognizable the next time.

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15
Q

How do phagocytes destroy pathogens?

A

Phagocytosis.

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16
Q

Where are phagocytes located?

A

̶ Blood
̶ Skin
̶ Mucous membranes
̶ Lymph

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17
Q

How does phagocytosis works?

A

The phagocytic cell notices a pathogen and engulfs it into a vacuole then fuses with a lysosome containing digestive enzymes. These digest the pathogen into bits and pieces and spits it out.

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18
Q

Parts of lymphatic system

A

Thymus. Peyer’s patches (in small intestine). Appendix
(cecum). Adenoid. Tonsils. Lymphatic vessels. Spleen
Lymph nodes (that swell when sick).

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19
Q

Lymphatic vessels is interconnected with what?

A

With blood capillaries.

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20
Q

Why do lipids go through the lymphatic system?

A

Because fats are too large.

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21
Q

Lymph nodes

A

Have lymphatic vessels lead into lymph node. Macrophages live permanently live in there. Masses of defensive cells are stored there and ready to be disposed when you have an inflection. They get to infected area through blood vessel capillary system. They also can put fluid that leak from circulatory system back to that system and also monitor it to make sure there is no pathogens in it (makes sure blood is clean before returned back).

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22
Q

Natural Killer Cells

A

Recognize surface proteins of virus-infected or
cancerous cells. They target them and release chemicals that cause apoptosis (cell death) in infected or cancerous cells.

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23
Q

Antimicrobial proteins

A

Attack pathogens or impede their reproduction. ie. interferons and complement proteins.

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24
Q

Interferons

A

A protein are secreted by virus-infected cells. Help surrounding cells from further inflected by the viruses. Trigger surrounding cells to produce chemicals that inhibit viral reproduction.

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25
Q

Complement Proteins

A

Found in blood plasma. Are plasma proteins activated (by many things) by substances on the surface of many microbes. When activated they from a structure that embeds into the cell membrane of pathogens and forms a little tube (hole) which allows fluid and salts to pass through, so it will burst open. Lead to lysis of invading cells. Also involved in inflammation and in adaptive immunity. Many proteins that come together when activated.

26
Q

Inflammatory Response

A

Signaling molecules released by injured or (flu) infected tissue (or white blood cells that are there) cause local inflammation (e.g., sore throat). ie. histamine and cytokines.

27
Q

Histamines

A

Triggers vasodilation (veins are dilating) and increased blood vessel permeability in affected area because the vessels walls are stretching and then they bring more blood to the area. More white blood cells and proteins can enter interstitial fluid. When you bring in more blood the area will become red.

28
Q

Cytokines

A

Further increase blood flow to the affected to bring in more white blood cells.

29
Q

Inflammatory Response steps

A

Signaling molecules cause capillaries to dilate (e.g., histamines) and increase blood flow (e.g., cytokines). The mast cells and macrophage release signing molecules to create a response. The phagocytic cells (e.g., neutrophils), activated complement proteins, and other antimicrobial proteins arriving from the blood work together to fight the infection.

30
Q

Long term Inflammatory Response

A

A serious (flu) infection can cause a systemic
inflammatory response (e.g., fever)
– Release more white blood cells from the bone
marrow (all blood cells are produced here) because you need a lot of them.
– Reset body’s thermostat to cause fever (enhances phagocytosis of white blood cells and speeds up the chemical reactions that and in tissue repair as well.

31
Q

Histamine increases local blood flow. This leads
to the arrival of blood cells that release cytokines that promote local blood flow this is an example of what?

A

positive feedback

32
Q

Adaptive immunity involves what?

A

pathogen-specific recognition (one on one).

33
Q

How is specificity achieved?

A

through interactions between antigens and antigen receptors.

34
Q

Antigens

A

large molecules found on the surface of specific
pathogens or secreted by those pathogens.

35
Q

Antigen receptors

A

proteins produced by B cells or T cells (white blood cells stored in the lymphatic system).

36
Q

Antigens contain what?

A

multiple epitopes

37
Q

Epitopes

A

An epitope is a small, accessible portion of an
antigen that binds to an antigen receptor (lock and key binding).

38
Q

An immune system that is able to recognize
multiple epitopes of a single antigen molecule is
advantageous because of what?

A

It is less likely that multiple epitopes will mutate than it is that one epitope will mutate.

39
Q

B cells and T cells are what?

A

lymphocytes

40
Q

Lymphocytes

A

White blood cells; produced in the bone marrow.
– B cells mature in the bone marrow.
– T cells migrate to the thymus for maturation.

41
Q

Each B or T cell produces a single type of what?

A

Antigen receptor. Each B cell will produce an antigen receptor that’s different than the next B cell. Same with T cell.

42
Q

Each antigen receptor binds to what?

A

a single epitope of a single antigen

43
Q

What produces the specificity of the antigen-
binding site?

A

Variable regions of antigen receptors.

44
Q

Physical structure of B and T cells?

A

They both have variable and constant regions. Also have antigen-binding site. But B cells have two and T cells have one.

45
Q

Humoral Response for B cells?

A

B cell antigen receptors bind to intact antigens in
the blood or lymph. These antigens may be on the surface of pathogens or may be free antigens secreted by pathogens.

46
Q

Cell-Mediated Response for T cells?

A

T cell antigen receptors can only bind to antigen
fragments presented on the surface of host cells. The pathogen wants to use the host to reproduce more of it, so it inflects the host cell and proteins from it are released. So antigen fragment has many copies ion the host cells. A MHC molecule then place a tag on one of them. This is now a displayed antigen fragment (a flag saying that it’s been inflected), this is where the T cell binds to.

47
Q

What do B and T cells do when they encounter their specific epitope?

A

Their cells proliferate (replicate themselves) and this takes some time. From there they become effector or memory cells.

48
Q

Effector cells

A

Short-lived cells that take effect immediately
against the pathogen or antigen. This is the first step.

49
Q

Memory cells

A

Long-lived cells that give rise to effector cells if
the same epitope is encountered again.
now you can tell you have already been effected. Responsible for long- term protection provided by a prior infection or vaccination.
Memory cells, produced during the original B cell
or T cell proliferation, give rise to effector cells if the
same epitope is encountered again (then make more effector cells). Secondary immune response ➔ rapid (because they don’t need to wait for B and T cells to proflierate.

50
Q

Effector forms of B cells

A

are plasma cells, which secrete antibodies

51
Q

Antibodies

A

soluble forms of the antigen receptor; specific for the same epitope as the original B cell. They release and float around the blood system. They will find floating pathogen and mark pathogens for inactivation or destruction. Neutralization prevents pathogen
entry into cells. Toxins can also be neutralized by
antibodies.

52
Q

Antibody binding increases what?

A

the ability of phagocytic cells to recognize the
pathogens. Leads to increased phagocytosis of
pathogens.

53
Q

Antibodies activate what?

A

complement system, leading to pore formation. Complement proteins attached to antibody, the formation of membrane attack complex, then flow of water and ions into the pore which burst the pathogen and kills it.

54
Q

Effector forms of T cells

A

helper T cells and cytotoxic T cells.

55
Q

Helper T cells

A

Attachs to antigen receptor. They go in and help other cells to dp their job. Tag themselves to inflected cell and then release cytokines (proteins that increase blood flow) and these will activate the production of more B cells and cytotoxic T cell.

56
Q

Cytotoxic T cells

A

secrete proteins that lead to cell death in infected cells. They also bind to infected cells and secrete perforin and granzymes, after this they will go fond another in

57
Q

Perforin

A

causes pores to form in the cell membrane of infected cells. Burst and die.

58
Q

Granzymes

A

initiate apoptosis (cell death).

59
Q

Is the conc. of antibodies higher the second time?