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Endo-Repro Midterm > Immunology > Flashcards

Immunology Flashcards

1
Q

What type of lymphocytes are involved in central and peripheral tolerance?

A
  • Central: developing lymphocytes

- Peripheral: mature lymphocytes

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2
Q

Where do both T and B cells develop?

A
  • T cells: thymus

- B cells: bone marrow

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3
Q

What is involved in T-cell central tolerance?

A

autoimmune regulator protein (AIRE): thymic cells express tissue-restricted antigen to educate T cells on periphery

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4
Q

What happens if there is a lack of AIRE? How does this relate to IDDM?

A
  • lack of AIRE = no negative selection (autoimmunity)

- IDDM -> insulin gene not expressed on AIRE -> autoimmunity to insulin

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5
Q

What population of cells handles T-cell peripheral tolerance? What do they secrete?

A

Tregs - secrete IL-10 and TGF-B to inhibit T cell and B cell inflammatory response

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6
Q

What 3 things are upregulated on Tregs that aren’t on any other cell type?

A
  • Foxp3: allows them to express CTLA-4 and CD25
  • CD25: high affinity IL-2 receptor
  • CTLA-4: high affinity for B7 -> beats out CD28 and T cells become anergic
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7
Q

What does the loss of Tregs/foxp3 lead to?

A

widespread autoimmunity

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8
Q

What is involved in B cell central tolerance that is unique to B cells?

A

receptor editing: expression of a new light chain region

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9
Q

What is the inhibitory receptor used in peripheral B tolerance?

A

Fc receptor on the surface of B cells -> binds to antibodies and shuts down internal B cell signaling

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10
Q

What is functional inactivation of B cells?

A

peripheral tolerance where B cell is activated but signaling not done properly - no involvement of complement or TLR -> anergy

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11
Q

Name 7 trigger/risk factors for NIDDM

A
  • microbiome: delivery; Abx
  • diet
  • energy expenditure
  • early life: placental function, postnatal growth
  • sleep debt
  • chronic inflammation
  • genetics: coupled w/ environment
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12
Q

What type of immune cells does lean adipose tissue largely contain?

A

contains Tregs, M2 macrophages (anti-inflammatory) and Th2 cells (suppressive)

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13
Q

Explain how necrosis can occur in adipocytes? What does this lead to?

A

adipose tissue is highly vascularized -> fat cells get larger (obesity) -> constrict vasculature -> necrosis -> inflammation

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14
Q

What is there in influx of when adipose tissue become inflamed?

A

M1 macrophages and acute phase cytokines (IL-1, IL-6, and TNF)

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15
Q

What does the inflammatory reaction in adipose tissue lead to (3)?

A
  • acute phase protein production from liver
  • hypothalamus inflammation
  • TNF -> vascular permeability -> leukocyte migration to area of inflammation
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16
Q

What affect does IL-6 have on each of the following: liver, skeletal muscle, adipose tissue, and GI tract?

A
  • liver: acute phase proteins and insulin resistance
  • skeletal muscle: increase GLUT4 translocation and lipolysis
  • adipose: increase lipolysis
  • GI tract: increase GLP-1 in intestine and pancreas
17
Q

What receptor is found on adipocytes and what can this lead to?

A

TLR4 found on adipocytes -> binds to palmitate (long chain FFA) -> pro-inflammatory response

18
Q

What types of immune cell changes occur in adipose tissues in obesity?

A
  • increase in M1 macrophages and CD8 T cells

- Decrease in M2 macrophages and Tregs

19
Q

What type of hypersensitivity is IDDM?

A

Type IV hypersensitivity - T cell mediated

20
Q

What other disease are IDDM pts likely to develop?

A

25% of developing Celiac disease

21
Q

Which HLA class II alleles are found in 90% of people w/ IDDM?

A

DQ2/DQ8

22
Q

Which HLA class II alleles are most common in children dx before age 5 w/ IDDM?

A

DR3/DR4

23
Q

Which HLA class II alleles are considered protective against IDDM?

A

DR2/DR6

24
Q

Which class of variable number tandem repeats (VNTR) increases the risk of IDDM?

A

Class I

25
Q

Which class of VNTR is associated w/ lower insulin mRNA synthesis? How does this lead to IDDM?

A

Class I - lower expression of insulin by thymocytes during T cell maturation

26
Q

What does a mutation in CTLA-4 lead to?

A

decreases ability to down-regulate immune response in the periphery and maintain tolerance

27
Q

What is the relationship between IDDM and breast feeding? Why?

A

not breast feeding (drinking cow’s milk) increases risk of IDDM -> cows milk contains less insulin than breast milk

28
Q

Which vitamin deficiency has been connected to increased risk of IDDM?

A

Vitamin D

29
Q

How does being born by C-section increase risk of IDDM?

A

infant doesn’t receive mother’s microbiome through vaginal delivery

30
Q

Which viruses have been implicated in IDDM?

A

mumps, rubella, cytomegalovirus, enteroviruses, retroviruses

31
Q

How do viruses lead to destruction of pancreatic B cells?

A
  • overlapping epitopes w/ pancreatic B cell antigens

- immune system appropriately activated against virus but can now also interact w/ pancreatic B cells and destroy them

32
Q

What is the main mechanism of destruction of pancreatic B cells?

A

CD8 T cell destruction using perforin and granzymes to induce apoptosis

33
Q

Explain the process of activation of the immune system against pancreatic B cells?

A

B cell damaged somehow -> presented by APC to CD8 T cells and Th1 cells -> CD8 T cell begin destroying them -> also cross presentation w/ CD4 T cells activating B cells and producing autoantibodies

34
Q

What confirms a diagnosis of IDDM?

A

presence of islet cell autoantibodies (ICAs)

35
Q

What are 3 ICAs that are tested for when looking for IDDM?

A
  • glutamic acid decarboxylase (GAD65)
  • insulinoma antigen-2 (IA-2)
  • insulin auto-antibodies (IAA)
36
Q

How does IDDM change the population of Tregs?

A
  • lose expression of foxp3
  • no longer secrete IL-10 and TGF-B
  • begin secreting INF-y and IL-17 (pro-inflammatory seen in autoimmune diseases)
37
Q

What could you give therapeutically to mitigate the loss of Tregs?

A

soluble CTLA-4 (short term tx)

Endo-Repro Midterm (3 decks)

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