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IHO FINAL > Immunology Part IV > Flashcards

Immunology Part IV Flashcards

1
Q

What types of cells recognize free antigen?

A

B cells

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2
Q

Do T cells recognize free antigen?

A

NO

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3
Q

What cytokines polarize Th1?

A

IFN-gamma, IL-12, IL-18

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4
Q

What cytokines does Th1 produce?

A

IFN-gamma, TNF

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5
Q

What happens after Th1 is activated?

A
  1. Daughter cells leave and circulate around the body.
  2. When the cells encounter antigens, they secrete lymphokines.
  3. Lymphokines released: IFN-gamma = pro-inflammatory, chemotactic agent for blood monocytes and tissue macrophages
  4. Tissue macrophages move in large numbers to area where Th1 recognizes antigen and are activated by IFN-gamma, becoming classically activated M1 (angry) macrophages [these ingest and kill bacteria and other foreign invaders]
    - Can cause damage to local tissues = contact sensitivity
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6
Q

What do macrophages release?

A

They release their own cytokines at the site of infection that intensify inflammation = TNF-alpha & IL-1

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7
Q

What cytokines polarize Th2?

A

IL-4

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8
Q

What cytokines does Th2 produce?

A

IL-4, IL-5, IL-13 (and IL-10)

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9
Q

What does IL-4 and IL-13 from Th2 cells cause?

A
  • IL-4 and IL-13 attracts and activates macrophages (alternatively activated = M2) which are involved in healing (debris removal, scar formation, walling off pathogens that angry macrophages have failed to kill)
  • IL-4 = chemotactic for eosinophils which are specialized to kill parasites like protozoans and worms
  • Appear later in sites of inflammation
  • Th2 cells also give rise to Tfh cells which migrate to lymphoid follicles.
  • Their high amounts of IL-4 push B cells to switch from naive IgM/IgD state to making IgE (parasite resistance & allergy)
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10
Q

What cytokines polarize Th17?

A

TGF-beta, IL-1, IL-6, IL-23

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11
Q

What effector cytokines are produced by Th17?

A

IL-17 and IL-22

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12
Q

What happens after Th17 is activated?

A
  • Main job seems to be to cause inflammation. Implicated in several autoimmune diseases (as have Th1 cells)
  • Aggressive pro-inflamamtory. Leads to accumulation of angry (classically activated) macrophages at the site of infection. It’s a vigorous response to get pathogens under control quickly
  • If it becomes chronic, it can result in significant tissue damage
  • Play their biggest role in maintaining integrity of mucosal surfaces
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13
Q

What surface markers are on Tfh?

A

CD4, CXCR5 (homing to follicles)

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14
Q

What cytokines polarize Tfh?

A

IL-6 and IL-21

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15
Q

What cytokines does Tfh produce?

A

IL-4 and IL-21

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16
Q

What do Tfh cells do when activated?

A
  1. Soon after arrival of AP-DC in lymph node, these Tfh cells can be seen migrating into follicles of cortex where there are a lot of B cells.
  2. They then help B cells that have recognized antigen become activated and differentiate into antibody-secreting plasma cells.
  3. Tfh cells secrete cytokines to direct the B cells to switch from secreting IgM, to IgG, IgA or IgE. [Tfh in gut switches B cells preferentially to IgA, Tfh in spleen switches B cells to IgG]
  4. Antibodies we make are as much an indication of T cell function as B cell function!
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17
Q

What are three surface makers on Treg cells?

A

CD4, CD25, CD127low

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18
Q

What cytokines polarize Treg cells?

A

IL-2 and TGF-beta

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19
Q

What effector cytokines do Treg cells produce?

A

IL-10 and TGF-beta

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20
Q

What is important to know about IL-2?

A

It’s a pro proliferative signals for Th cells in general!

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21
Q

What do Treg cells do?

A
  • Only 5% of Th cells
  • Suppress activation and function of all other Th cells!
  • Best defined as “anti helpers”
  • Produce TGF-beta and IL-10 and are very potent (1 Treg suppress 1000 other cells)
  • People who lack Treg get autoimmune disease = IPEX
22
Q

What is the process of T cell maturation in the cortex?

A

Positive selection - Does it recognize self MHC? No - dies by neglect
Negative selection - Does it recognize self antigen? Yes - dies

23
Q

How many T cell survive positive and negative selection?

A

2%

24
Q

What happens if TCR self affinity (MHC) is too low?

A
  • Fail to be positively selected
  • “Death by neglect”
  • 90-96% of all T cells
25
Q

What happens if TCR self affinity (antigen) is too high?

A
  • Negatively selected
  • Deleted
  • 2-5%
26
Q

What happens with TCR self affinity that is intermediate (good)?

A
  • Positively selected
  • Survive
  • 2-5%
27
Q

A T cell must:

A
  1. Not recognize “self” antigen. Cannot bind so firmly to a self structure (MHC alone, or MHC loaded with ‘self’ peptide) that the T cell becomes activated; this would be autoimmunity (negative selection)
  2. Not recognize free antigen (which is antibody’s job)
  3. Recognize antigenic peptide plus self MHC (positive selection)
    This repertoire is selected within the thymus.
28
Q

MHC Polymorphism: HLA-B27?

A

90X more likely to develop spondylitis (destruction of vertebral cartilage)
-Also linked to psoriasis, inflammatory bowel disease, and Reiter’s syndrome

29
Q

MHC Polymorphism: HLA-DR2?

A

130X more likely to develop narcolepsy

-Also linked to multiple sclerosis, hay fever and SLE

30
Q

MHC Polymorphism: HLA-A3/B14?

A

90X more likely to develop hemochromatosis (too much iron adsorption which can lead to internal organ damage)

31
Q

MHC Polymorphism: HLA-DQ2/GQ8?

A

Linke to Celiac Disease

32
Q

MHC Polymorphism: HLA-DR3?

A

Linked to diabetes mellitus type I, Grave’s disease

33
Q

MHC Polymorphism: HLA-DR4?

A

Linked to RA and diabetes mellitus type I

34
Q

MHC Polymorphism: HLA-B53?

A

Associated with protection against childhood malaria

  • Specific global distribution pattern:
  • -Gene frequency in Ghana = 40%
  • -Gene frequency in China & South Africa = 1-2%
35
Q

What molecular interactions take place between T cells (CD8 or CD4) and APCs?

A
  • LFA-1 on T cell binds ICAM-1 on APC
  • CD28 on T cell binds B7 (CD80/86) on APC
  • TCR (CD3 + CD4/CD8) binds MHC I/II on APC
  • CD2 on T cell binds LFA-3 on APC
36
Q

Where does antigen come from on MHC I and MHC II?

A

MHC I - from inside the cell

MHC II - from the surrounding area/outside the cell

37
Q

How do APCs uptake antigen?

A

DC - Endocytosis, Phagocytosis
Macrophage - Phagocytosis
B cell - Receptor-mediated endocytosis

38
Q

How do APCs get activated?

A

DC - Mediated by PRRs
Macrophage - Mediated by PRRs and enhanced by T cell help
B cell - Mediated by antigen recognition

39
Q

How does MHC Class II expression change in APCs?

A

DC - Constitutively expressed, Inc. with activation (may express low levels constitutively)
Macrophage - Must be induced, Inc. with activation
B cell - Constitutively expressed, Inc. with activation (express low levels of constitutively)

40
Q

What costimulatory activity do APCs do?

A

DC - Constitutively express, Up-reguatlion of CD80/86 with activation
Macrophage - Must be induced, Up-regualtion of CD80/86 with activation
B cell - Must be induced, Up-regualtion of CD80/86 with activation

41
Q

What T cells do APCs activate?

A

DC - Naive T cells, Effector T cells, Memory T cells
Macrophage - Effector T cells, Memory T cells
B cell - Effector T cells, Memory T cells

42
Q

What MHC class is associated with the Cytosolic pathway? What MHC class is associated with the Endocytic pathway?

A

Cytosolic - MHC Class I

Endocytic - MHC Class II

43
Q

What is the process of presenting antigen through the Cytosolic/Endogenous Pathway?

A
  1. Endogenous protein is ubiquinated
  2. Protein goes to proteasome to be degraded
  3. After degradation, peptides are transported to RER via TAP where Class I molecules are synthesized.
  4. Peptides then bind to the transporter protein heterodimer complex (TAP1 and TAP2). This complex extends across the RER membrane and facilitates the passage of these peptides to the lumen of the RER where loading of the peptides to Class I molecules can take place.
  5. Tps (tapasin) allows for the association with TAP 1/2 complex.
  6. MHC Class I associated with calnexin to ensure proper folding. Once folded properly, it associated with B2-microglobulin –> release of calnexin.
  7. Peptide added, ERAAP trimming may occur not eh way to the MHC Class I molecule.
  8. MHC Class I is released and transmits to surface of the cell.
44
Q

What is the process of presenting antigen through the Endocytic/Exogenous Pathway?

A

-Requires ENDOCYTIC uptake of EXOGENOUS antigen.
1. Antigens are internalized into APCs through endocytosis/phagocytosis in clathrin-coated vesicles. DC and macrophage tend to phagocytize stuff. B cells use receptor mediated endocytosis.
2. Internalized antigens are degraded in phagolysosomes or endosomes.
3. Antigenic peptides are associated with MHC Class II molecules on the cell surface.
A. MHC Class II molecules are assembled by the invariant chain binding first
B. Assists in the folding of MHC Class II alpha and beta chains, binds to peptide-presenting site of the Class II molecules and assists in the transport of the MHC Class II molecules from the Golgi to the cytoplasmic vesicles
C. Then, the invariant chain is digested and you’re left with CLIP in the MHC Class II.
D. A nonclassical Class II MHC molecule is required to catalyze the exchange of antigenic peptide for the CLIP = HLA-DM. HLA-DM can be regulated by HLA-DO.
5. Last a peptide is added that replaces CLIP, which is released

45
Q

What is TAP1/TAP2?

A

Transporter protein heterodimer complex (TAP1 and TAP2). This complex extends across the RER membrane and facilitates the passage of peptide into the lumen of the RER where they can be loaded onto MHC Class I. (Endogenous/cytosolic pathway)
-TAP = Transporter associated with antigen processing. Has affinity for peptides 8-16 amino acids long.

46
Q

What is ERAAP?

A

Does final trimming of peptides from TAP 1/2 in the ER. [ER associated amino peptidase] Trimming may occur on the way to the MHC Class I molecule.

47
Q

What is Calnexin?

A

As the MHC Class I is being created, it associates with calnexin to ensure proper folding. Once folded properly, it associates with B2-microglobulin –> release of calnexin.

48
Q

What is the invariant chain?

A

Assists in folding of MHC Class II alpha and beta chains, binds to the peptide-presenting site of the Class II molecules, and assists in the transport of the MHC Class II molecules from the Golgi to the cytoplasmic vesicles.

49
Q

What is CLIP?

A

Short fragment bound to the antigen presenting site o the MHC Class II molecule (CLIP = Class II-associated invariant chain peptide)

50
Q

What is HLA-DO?

A

HLA-DM can be regulated by HLA-DO. Only expressed in B cells and in the thymus. It blocks HLA-DM except in very acidic conditions.

51
Q

What is HLA-DM?

A

A nonclassical Class II MHC molecule required to catalyze the exchange of antigenic peptide for CLIP

IHO FINAL (12 decks)

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