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Pathophys > T-Cells > Flashcards

T-Cells Flashcards

1
Q

T-cells always have a T-cell receptor which is similar to an antibody but not in what three ways?

A
  1. Not free floating
  2. Only one binding site
  3. Wants it’s antigen handed to it.
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2
Q

What two things have to be right for binding to a T-Cell receptor?

A

Right Antigen

Right MHC.

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3
Q

Is the binding domain for a T-cell made the same way that binding domains are made for antibodies?

A

Yes, DNA for the binding domain is randomly mutated.

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4
Q

How many MHCs do we have? How many from mom and How many from dad?

A
  1. 12

2. 6 and 6.

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5
Q

What two classes of MHCs do we have?

A

Class I and II

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6
Q

Class I MHCs contain which three? How many legs do they have?

A
  1. A B and C

2. one leg

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7
Q

Class II MHCs contain which three? How many legs do they have?

A

1, DR, DP and DQ

2. two legs

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8
Q

What do Class I and Class II MHCs do?

A

Present antigen to T-cell receptors.

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9
Q

Why do we have two classes of MHCs?

A

To prevent two very different kinds of antigens.

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10
Q

In Class I MHCs, every time the cell makes a protein it sends some out to get quality reviewed, chopped up and presented on a MHC. These are self proteins. Why are we doing this?

A

The antigen is self-protein. This is for viruses. If virally infected we could end up making viral proteins. So if they are chopped up and then we have something that reacts with it then we kill it. Cancer acts the same way with mutant proteins or proteins at a way high rate.

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11
Q

What does a class II MHC present? Do we kill this cell?

A

Finds a protein, chops it up and presents it. Don’t want to kill the cell because it is not intracellular. W

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12
Q

When will macrophages and B-cells endocytose self-protein? What happens to T-Helper cells?

A

In times of necrosis.

T-helper cells won’t activate.

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13
Q

Class I MHCs are present on what kind of cells?

A

All nucleated cells and platelets

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14
Q

Class II MHCs are present on which kind of cells?

A

Bcells, APC, and some epithelial cells

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15
Q

Which class of MHC presents endogenous antigens from intracellular proteins?

A

Class I

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16
Q

Which class of MHC presents exogenous antigens from digested extracellular pathogens?

A

Class II

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17
Q

Class I MHCs react with what?

A

CD8 on Cytotoxic T cells

18
Q

Class II MHCs react with what?

A

CD4 on T helper cells.

19
Q

Is CD8 Cytotoxic or Helper? What about CD4?

A

CD8- Cytotoxic

CD4- Helper

20
Q

When a virus presents a “home grown protein” the T cells react with it meaning it’s foreign and the cytotoxic T-cell asks it to do what?

A

To do apoptosis

21
Q

TH1 Helper cells respond to what?

A

Macrophages presentation

22
Q

TH2 Helper cells respond to what?

A

B-Cells

23
Q

When do TH1 and TH2 differentiate and when do they become active?

A

They are not active until they find their cell and they also don’t know what they are until they find their cell.

24
Q

What hangs out for a long time and grabs whatever it finds and then runs to the lymph nodes?

A

Dendritic cells.

25
Q

What kind of selection do we want in the thymus for our T-cells?

A

We want negative and positive selection

26
Q

Why do we want both negative and positive selection while manufacturing T-cells in the thymus?

A

Want somebody who is interested but not too interested. We want them to interact with our MHCs. If they can’t talk to our MHCs they are worthless. Show them bare MHCs. This is where we decide whether they are a CD8 or CD4. IF you don’t interact with any of those then they get thrown away. Anything that binds too tightly is a stalker- we get rid or these.

When we are done we have T cells that have been classified as CD4 or CD8 and they aren’t self reactive but they can bind to MHC.

27
Q

What do we mean by immune privileged sites? What areas does this include?

A

Places where T-cells are not allowed to go.
Placenta/fetus- half of the DNA in there is foreign.
Testes and ovaries- when these start working at their respective times they start making proteins that have never been made before. We could end up with self-reactive proteins
Thymus- we don’t want mature T-cells to come where we are training new ones
Eyes-so important and infected so rarely that we leave them alone. Injure one eye and we end up with an immune response to both. Sympathetic blindness causes blindness in the unaffected eye because of the damage in the other.
Brain- if we kill a virus in the neurons then we don’t get a new one. Fever sores don’t erupt under normal circumstances because the immune system kills it any time the virus attempts to leave the neurons. When we are immunocompromised or using our immune system elsewhere they can get out of the neurons and not immediately get killed causing fever sores.

28
Q

When lymph nodes enlarge, what part is getting bigger? What does it contain? What happens in the lymph node?

A

Germinal centers get bigger and bigger when lymph nodes enlarge. Germinal centers are filled with B-cells. Secondary lymphoid tissue is where we concentrate the antigen

29
Q

Are dendritic cells warriors? What do they do? If the dendritic cell is not the warrior who is?

A

Dendritic cells are not warriors. Find a severed part, goes back to the lymph node and looks for the Helper T-cell that is excited by it, makes a ton of copies and then the copies go to help.
Macrophage is the warrior.

30
Q

When do NK cells come into play?

A

If the cell doesn’t make MHC, NK cells just looks at their papers (doesn’t read just looks) and if they look okay they live, if they look bad they die. The NK cell releases granule contents including apoptosis in the target cell.

31
Q

Describe a the difference between how a MHC class II molecule and a superantigen bind to a T-cell Receptor?

A

The T-cell receptor and a MHC class II molecule normally simultaneously interact with a processed antigen to induce T-cell differentiation. Superantigens bind directly to the side of the TCR and to the MHC class II molecules activating Th cells independent of TCR antigen specificity. Much less specific, binds tightly to a ton of cells causing an over active immune response.

32
Q

How many types of hypersensitivity are there?

A

4.

33
Q

When is a type II hypersensitivity common? What is the immune reactant?

A

Blood transfusions, Graves disease (TSH receptors) myasthenia gravis (ACh receptors)
IgG

34
Q

When IgE binds to our mast cells to fight off something that isn’t even that big of a threat what kind of a hypersensitivity is this? Name a couple examples

A

Type I

Allergic rhinitis, systemic anaphylaxis, asthma

35
Q

What is happening in a type III hypersensitivity?

A

Lots of debris and antibody so we end immune complexes (from the antigen in the blood and antibody) we have way more than we should have. They get deposited on the walls of blood vessels and then when cells come to get rid of them they damage the vessels.

36
Q

How many types of Type IV hypersensitivity are there? What mediates them?

A

3.

T-cell mediated.

37
Q

In a Type I IgE mediated hypersensitivity are most of the disease allergy, autoimmunity or alloimmunity related? Name three of the most common.

A

Allergy (environmental antigens)
Allergic rhinitis
Anaphylaxis
Astha

38
Q

What is the most common type of Type II (tissue specific) hypersensitivity? What two diseases are included in this? Name other diseases caused by Type II hypersensitivities.

A

Most common is autoimmunity (self antigens) including Graves and Myasthenia Gravis.

Rarely an allergy to PCN causing hemolysis causes a Type II hypersensitivity

Bad blood transfusions, hemolytic disease of the newborn and hyperacute graft rejection are alloimmunity related types of Type II hypersensitivity.

39
Q

In Type III (immune complex) hypersensitivies, what are the five diseases? What subtype are they classified into and which one is rare?

A

Type III Allergy- wheat gluten
Type III autoimmunity- Lupus and necrotizing vasculitis
Type III Alloimmunity: serum sickness

Rare is the wheat gluten allergy.

40
Q

What are the most common Type IV T-cell mediated hypersensitivities? What other two are included under Type IV.

A

Most common are autoimmunity related hashimotos thyroiditis and type 1 DM

Type IV allergy related includes poison ivy
Type IV alloimmunity related includes transplant rejection.

41
Q

Why are steroids used in Type I hypersensitivity reactions?

A

Prevent rebound reactions.

42
Q

Are autoimmune diseases predisposition or destiny?

A

Predisposition including inheritance of susceptibility genes that may interfere with self tolerance, and environmental triggers that promote lymphocyte entry into tissue, activation of self-reactive lymphocytes and tissue injury.

Pathophys (5 decks)

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