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Year 2 MIS > Mechanism of autoimmune diseases > Flashcards

Mechanism of autoimmune diseases Flashcards

1
Q

What is the term used to describe when the immune system fails to distinguish between self antigens and foreign antigens?

1 - breach of immunity
2 - breach of self tolerance
3 - reactive immunity
4 - self immunity

A

2 - breach of self tolerance

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2
Q

In immunity what does positive and negative selection refer to?

A
  • positive = B and T cell receptors bind their ligand

- negative = B and T cell receptors bind self antigens and undergo apoptosis

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3
Q

What is central tolerance?

A
  • screening of B and T cells to ensure they are not self reactive
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4
Q

Peripheral tolerance is essentially the elimination of B and T cells in peripheral tissues that are self reactive. T-regulatory cells are one mechanism of peripheral tolerance. What is the function of T-regs?

A
  • specialised T cells that can inhibit the response of all other immune cells
  • generally as part of peripheral tolerance
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5
Q

Peripheral tolerance is essentially the elimination of B and T cells in peripheral tissues that are self reactive. Clonal anergy is one mechanism of peripheral tolerance. What is clonal anergy (which is latin for without)?

1 - Treg cells inhibit T cells
2 - inhibiting APC from presenting antigens on MHC-II to T cells
3 - inhibiting the 2nd stimulation required for T cell activation
4 - inducing apoptosis of T cells

A

3 - inhibiting the 2nd stimulation required for T cell activation

  • no binding of CD28 on T cell and B7 on APC
  • inactivating lymphocytes that are specific to a self antigen
  • inhibit co-stimulation so don’t get full activation
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6
Q

Peripheral tolerance is essentially the elimination of B and T cells in peripheral tissues that are self reactive. Peripheral deletion, also called clonal deletion is one mechanism of peripheral tolerance. What is peripheral deletion?

1 - self reactive T cells do not receive 2nd stimulus and APC cells induce apoptosis
2 - self reactive T cells do not receive 2nd stimulus and cytotoxic T cells induce apoptosis
3 - self reactive T cells do not receive 2nd stimulus and up-regulate Fas
4 - self reactive T cells do not receive 1st or 2nd stimulus for activation

A

3 - self reactive T cells do not receive 2nd stimulus and up-regulate Fas
- Fas is a ligand that can induce apoptosis in T cells as the immune response is reducing

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7
Q

What does autoimmunity refer to?

A
  • immune system responds to self-antigens

- a failure of self tolerance (ability not to respond to antigen that are not harmful)

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8
Q

What does autoimmune disease mean?

A
  • adaptive immune response to self antigen, leading to tissue damage
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9
Q

What does tolerance mean?

A
  • state of non-reactivity to an antigen
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10
Q

The Coombes and Gell classification system can help distinguish whether an antibody is clearly pathogenic in a type II hypersensitivity. Which of the following is the 1st of the 3 criteria set out by the Coombes and Gell classification system?

1 - transfer of disease at birth only
2 - transfer of disease by infusion of serum, or during gestation
3 - disease cannot be transfer at birth but can via serum
4 - disease can be transferred via infusion of serum

A

2 - transfer of disease by infusion of serum, or during gestation

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11
Q

The Coombes and Gell classification system can help distinguish whether an antibody is clearly pathogenic in a type II hypersensitivity. Which of the following is the 2nd of the 3 criteria set out by the Coombes and Gell classification system?

1 - removal of antibody by plasmapheresis is beneficial
2 - removal of serum is beneficial
3 - addition of antibodies is beneficial
3 - addition of blood transfusion is beneficial

A

1 - removal of antibody by plasmapheresis is beneficial

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12
Q

The Coombes and Gell classification system can help distinguish whether an antigen is clearly pathogenic in a type II hypersensitivity. Which of the following is the 3rd of the 3 criteria set out by the Coombes and Gell classification system?

1 - pathogenic antibody can be isolated in immune complex
2 - pathogenic antibody is not present
3 - pathogenic anantibody can be identified and characterised
4 - pathogenic antibody is present

A

3 - pathogenic antibody can be identified and characterised

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13
Q

What autoimmune condition results in death of RBCs?

1 - thrombocytopenia
2 - sepsis
3 - neutropenia
4 - autoimmune haemolytic anaemia

A

4 - haemolytic anaemia

- type II hypersensitivity

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14
Q

Autoimmune haemolytic anaemia is a condition resulting in the death of RBCs. What happens to cause the RBCs to become auto-reactive?

1 - antibodies bind RBCs and highlight for phagocytosis or complement pathway
2 - antibodies bind RBCs and up-regulate inflammatory cytokines to damage RBCs
3 - antibodies bind RBCs and inhibit ability to carry O2
4 - antibodies bind RBCs and trigger sickle cell anaemia

A

1 - antibodies bind RBCs and highlight for phagocytosis or complement pathway

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15
Q

Autoimmune haemolytic anaemia is a condition resulting in the death of RBCs. Here antibodies bind to RBCs (could be from a blood transfusion) which primes the RBC for destruction as part of the immune response. What are the 2 methods of how the RBCs can be killed?

1 - complement activation and phagocytosis
2 - complement activation and clonal analgy
3 - phagocytosis and clonal analgy
4 - phagocytosis and clonal deletion

A

1 - complement activation and phagocytosis

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16
Q

Autoimmune haemolytic anaemia is a condition resulting in the death of RBCs. Here antibodies bind to RBCs (could be from a blood transfusion) which primes the RBC for destruction as part of the immune response. The RBCs can be destroyed via complement activation and phagocytosis. There is another condition that can be causes through the same mechanism, but this affects platelets, what is this called?

1 - lupus
2 - thrombocytopenia
3 - haemophilia
4 - anaemia

A

2 - thrombocytopenia

- destruction of platelets

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17
Q

What is Graves disease?

A
  • a type II hypersensitivity autoimmune disease targeting thyroid gland
  • likely to be due to TSH receptor antibodies
  • causes a form of hyperthyroidism
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18
Q

Graves disease accounts for 75% of autoimmune caused hyperthyroidism and is a type II hypersensitivity. What happens in graves disease to cause hyperthyroidism?

1 - IgG auto-antibody binds TSH receptor inducing apoptosis of the receptor
2 - IgG auto-antibody binds TSH receptor blocking receptor, but acts as TSH
3 - IgE auto-antibody binds TSH receptor blocking receptor and inhibit TSH
4 - IgM auto-antibody binds TSH receptor blocking receptor, but acts as TSH

TSH = thyroid stimulating hormone

A

2 - IgG auto-antibody binds TSH receptor blocking receptor, but acts as TSH
- TSH then causes hyperthyroidism

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19
Q

What is Hashimots thyroiditis?

A
  • an autoimmune disease that causes hypothyroidism

- think H for Hypo and Hashitmoto

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20
Q

Hashimots thyroiditis is a type IV hypersensitivity autoimmune disease that causes hypothyroidism. Although the exact cause is unknown, what 2 things does the immune system begin creating antibodies against in the thyroid?

1 - follicular cells and perioxidase
2 - follicular cells and thyroglobulin
3 - thyroglobulin and perioxidase
4 - perioxidase and TSH receptors

A

3 - thyroglobulin and perioxidase

- both essentially reduce the production of T3 and T4

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21
Q

What type of hypersensitivity is myasthenia gravis?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

2 - type II hypersensitivity

  • IgG or IgM antibodies bind directly to ACh receptors at post synapse
  • ACh cannot bind and no excitation of post synapse
22
Q

Myasthenia gravis is a type II hypersensitivity is where IgG or IgM antibodies bind directly to ACh receptors at post synapse and block ACh. What common symptoms does this present with?

A
  • eyes are often the 1st sign of disease
  • muscle weakness
  • fatigue
  • ptosis
  • facial muscle weakness (chewing, talking etc..)
23
Q

Spontaneous Urticaria (hives, nettle rash etc..) is an autoimmune disease. What type of hypersensitivity is this and how can this present?

A
  • type I hypersensitivity
  • associated with IgE antibody
  • common and distressing skin condition
  • can cause swelling and hives
24
Q

Spontaneous Urticaria is an autoimmune disease, causing a common and distressing skin condition that results in swelling and hives. How is this condition caused?

1 - IgM Fc3R1 antibodies cross-link on mast cells
2 - IgD Fc3R1 antibodies cross-link on mast cells
3 - IgA Fc3R1 antibodies cross-link on mast cells
4 - IgE Fc3R1 antibodies cross-link on mast cells

A

4 - IgE Fc3R1 antibodies cross-link on mast cells

- IgE because it is a type I hypersensitivity

25
Q

What type of hypersensitivity is Hashimotos disease?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

4 - type IV hypersensitivity

- T cell mediated

26
Q

Hashimotos disease is the most common cause of hypothyroidism in industrial cities, generally due to a deficiency in iodine.

  • True
  • False
A
  • True
27
Q

Hashimotos disease is the most common cause of hypothyroidism in industrial cities, generally due to a deficiency in iodine. Women are more commonly affected at what age?

1 - >30 y/o
2 - >40 y/o
3 - >50 y/o
4 - >75 y/o

A

1 - >30 y/o

28
Q

Hashimotos disease is the most common cause of hypothyroidism in industrial cities, generally due to a deficiency in iodine. Women >30 y/o are more commonly affected. Which 2 cells enter the thyroid organ causing tissue damage?

1 - CD8 T cells and B cells
2 - CD4 T cells and B cells
3 - CD4 and CD8 T cells
4 - macrophages and B cells

A

3 - CD4 and CD8 T cells

- target peroxidase and thyroglobulin

29
Q

What is autoimmune polyglandular syndrome, candidiasis, and ectodermal dystrophy?

1 - type II hypersensitivities affecting glandular tissue
2 - type III hypersensitivities affecting glandular tissue
3 - type IV hypersensitivities affecting glandular tissue
4 - rare genetic autoimmune disease affecting glandular tissue

A

4 - rare genetic autoimmune disease affecting glandular tissue

30
Q

What is the role of autoimmune regulator (AIRE) located in lymphoid tissue in central tolerance?

A
  • checks B and T cell receptors for self tolerance

- if they react to self antigens they undergo apoptosis or become T-reg cells

31
Q

The autoimmune regulator (AIRE) is located in lymphoid tissue. It is able to produce multiple proteins that are self antigens that can then be checked against B and T cell receptors for self tolerance. If they react to self antigens (negative selection) they undergo apoptosis or become T-reg cells. Autoimmune polyglandular syndrome, candidiasis, and ectodermal dystrophy is a rare genetically inherited disease caused by mutations to the AIRE gene. How is this generally transmitted?

1 - autosomal dominant
2 - autosomal recessive

A

2 - autosomal recessive

  • it is rare so you would need 2 versions of mutated gene
  • negative selection does not occur in this disease and self-reactive B and T cells pass central tolerance
32
Q

Candidiasis is a key feature of autoimmune polyglandular syndrome, candidiasis, and ectodermal dystrophy. What is candidiasis?

1 - fungal infection caused by bacteria
2 - viral infection caused by herpes
3 - bacterial infection caused by E.coli
4 - fungal infection caused by yeast

A

4 - fungal infection caused by yeast

- antibodies to IL-17 are produced

33
Q

What is DiGeorge syndrome?

1 - a rare genetic mutation caused by micro-deletions in chromosome 22
2 - type III hypersensitivity affecting muscles of the face and neck
3 - aggressive form of type IV hypersensitivity affecting muscles of the face and neck

A

1 - a rare genetic mutation caused by micro-deletions in chromosome 22

34
Q

DiGeorge syndrome is a rare genetic mutation caused by micro-deletions in chromosome 22. How can this lead to an autoimmune disease?

1 - thyroid does not develop
2 - thymus undergoes aplasia (atrophy)
3 - B cells do not develop so no antibodies
4 - hypothalamus is affected and does not release TSH

TSH = thyroid stimulating hormone

A

2 - thymus undergoes aplasia (atrophy)

- leads to T cell deficiency

35
Q

What is Immune dysregulation, polyendocrinopathy, enteropathy, X-Linked?

1 - disease causing a deficiency in central tolerance
2 - disease causing a deficiency in FOXP3 gene and no Treg cells
3 - disease causing a deficiency in peripheral tolerance
4 - disease causing a deficiency in AID gene

FOXP3 = factor forkhead box p3
AID = Activation-induced cytidine deaminase
A
  • 2 - disease causing a deficiency in FOXP3 gene and no Treg cells
  • rare monogenic primary immunodeficiency (PID), characterised by multi-organ autoimmunity
  • mutations in the transcription FOXP3, the master gene of T regulatory (Treg) cells
  • even if T cells are self reactive there is no Treg cells to inhibit or stop them as part of peripheral tolerance
36
Q

Immune dysregulation, polyendocrinopathy, enteropathy, X-Linked is a rare monogenic primary immunodeficiency (PID), characterised by multi-organ autoimmunity. It is caused by mutations in the transcription factor forkhead box p3 (FOXP3), the master gene of T regulatory (Treg) cells. What are the 3 key clinical features of this disease?

1 - inflammatory bowel disease, dermatitis, organ-specific autoimmunity
2 - coeliacs, dermatitis, organ-specific autoimmunity
3 - inflammatory bowel disease, rhabdomyolysis, organ-specific autoimmunity
4 - inflammatory bowel disease, dermatitis, systematic organ failure

A

1 - inflammatory bowel disease, dermatitis, organ-specific autoimmunity

37
Q

Which chromosome are the genes for the MHC-I and II molecules on?

1 - chromosome 2
2 - chromosome 3
3 - chromosome 6
4 - chromosome 8

A

3 - chromosome 6

38
Q

All 3 genes for the MHC-I molecules begin with HLA (human leukocyte antigen) contain one letter after the HLA, what are the 3 letters?

1 - HLA - A, HLA - B, HLA - D
2 - HLA - B, HLC - B, HLA - D
3 - HLA - A, HLA - B, HLA - C
4 - HLA - B, HLA - C, HLA - E

A

3 - HLA - A, HLA - B, HLA - C

- think MHC-I has only one letter

39
Q

All 3 genes for the MHC-II molecules begin with HLA (human leukocyte antigen) contain two letters after the HLA, what are the 3 letters?

1 - HLA - DP, HLA - DQ, HLA - DR
2 - HLA - DB, HLC - DP, HLA - DQ
3 - HLA - DA, HLA - DB, HLA - DQ
4 - HLA - DB, HLA - DC, HLA - DE

A

1 - HLA - DP, HLA - DQ, HLA - DR

40
Q

What isCoeliac disease?

A
  • immune-mediated small intestinal (SI) enteropathy (intestinal disease)
  • triggered by exposure to dietary gluten in genetically predisposed individuals, leading to malabsorption
41
Q

Coeliac disease is caused by a protein called gluten, what specific part of gluten is associated with coeliac disease?

1 - glutenin
2 - gliadin
3 - fructose
4 - galacatose

A 
2 - gliadin
- class of proteins present in wheat and several other cereals
42
Q

Although there is likely to be multiple causes of coeliac disease, 35% of total genetic risk factor is associated with MHC-II class proteins encoded by which human leukocyte antigen (HLA)?

1 - HLA-DQ2 and HLA-DR2
2 - HLA-DQ2 and HLA-DQ8
3 - HLA-DQ3 and HLA-DQ6
4 - HLA-DQ2 and HLA-DQ4

A

2 - HLA-DQ2 and HLA-DQ8

  • remember 8 / 2 = 4
  • MHC-II molecules need CD4
43
Q

Which virus has been shown to increase the risk of coeliac disease?

1 - herpes
2 - flu
3 - rotavirus
4 - bronchitis

A

3 - rotavirus

- generally causes GIT symptoms

44
Q

Gliadin is able to be absorbed by the small intestines and enter the lamina propria. Once into the lamina propria the enzyme tissue transglutaminase (tTG) removes the amide group producingdeaminated gluten protein. What happens to thedeaminated gluten proteins?

1 - they bind to epithelial cells and cause tissue damage
2 - they bind with B cells directly
3 - phagocytosed by macrophages and presented on MHC-II to T cells
4 - phagocytosed by macrophages and presented on MHC-I to T cells

A

3 - phagocytosed by macrophages and presented on MHC-II to T cells

45
Q

Once deaminated gluten proteins have been phagocytosed by macrophages and presented on MHC-II. What immune cells bind to MHC-II?

1 - cytotoxic CD8 T cells
2 - CD4 T helper cells
3 - B cells
4 - APC

A

2 - CD4 T helper cells

46
Q

Once deaminated gluten proteins have been phagocytosed by macrophages and presented on MHC-II CD4 T helper cells bind to the MHC-II. What happens after this?

1 - T cells phagocytose the APC
2 - T cells bind with B cells and start secreting antibodies
3 - T cells begin secreting inflammatory cytokines
4 - T cells undergo autocrine signalling, inducing clonal expansion

A

3 - T cells begin secreting inflammatory cytokines

-inflammatory cytokines can damage intestinal lumen

47
Q

Once deaminated gluten proteins have been phagocytosed by macrophages and presented on MHC-II CD4 T helper cells bind to the MHC-II and secrete inflammatory cytokines that can damageintestinal lumen. What 2 other cells are activated by T-helper cells?

1 - B cells and macrophages
2 - B cells and neutrophils
3 - B cells and Natural killer cells
4 - neutrophils and natural killer cells

A

3 - B cells and Natural killer cells

48
Q

Once B cells have been activated by CD4 T helper cells, what 3things can they then produce?

A

1 -anti-tissue transglutaminase (tTG) IgA
2 - anti-gliadin IgA
3 -anti-endomysial (smooth muscle bundles of many tissue)

49
Q

In coeliacs disease what 3 things happens to the GI walls?

A
  • villous atrophy
  • crypt hyperplasia
  • lymphocyte infiltration
50
Q

What type of hypersensitivity is coeliacs disease?

1 - type I hypersensitivity
2 - type II hypersensitivity
3 - type III hypersensitivity
4 - type IV hypersensitivity

A

4 - type IV hypersensitivity

Year 2 MIS (48 decks)

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