4 Adaptive Immune Diseases

Question 1

What two things cause autoimmune disorders?

Answer 1

genetics and the environment (or both)

Question 2

What rate of people with predisposing genes develop an autoimmune disorder?

Answer 2

about 20% have genetic issues that then become ‘activated’ by an environmental source

Question 3

Infectious and non-infectious causes for autoimmune diseases account for what percentage of all AI disorders?

Answer 3

80%

Question 4

What influences autoimmune disorder development?

Answer 4

HLA subtypes (part of TCR development on T-cells)

Question 5

What cells are closely tied to AI disorders?

Answer 5

CD4 T cells

Question 6

Which class of alleles are most frequently implicated in AI disorders?

Answer 6

Class II alleles, which means that CD4 T cells will also play a role in the disorder

Question 7

What primarily mediates Type II autoimmune diseases?

Answer 7

IgG or IgM

think back to Type II hypersensitivity

Question 8

Because IgG and IgM are mediators in Type II AI diseases, what are they targeting?

Answer 8

Cell surface proteins/antigens

Question 9

Antigens can either be _________ (stimulatory) or _________ (inhibitory)

Answer 9

agonist, antagonist

Question 10

What are some examples of Type II AI disorders

Answer 10

Type2 diabetes, Grave’s disease, hemolytic anemia, thrombocytopenia purpura, Hypoglycemia, Myasthenia Gravis

Question 11

Streptococcus pyogenes uses what to cause rheumatic fever?

Answer 11

mimicry: it shares the same surface epitopes as human cell epitopes

Question 12

What isn’t recruited to the site of infection during rheumatic fever?

Answer 12

T cells, making the infection transient

Question 13

What receptor is targeted against in Grave’s disease?

Answer 13

The thyroid stimulating hormone receptor (TSH receptor)

Question 14

If antibody response doesn’t cause autoimmune damage in grave’s disease, what does?

Answer 14

The TSH receptor is targeted by antibodies, which then stimulates the thyroid to increase metabolism (hyperthyroidism)

Question 15

What cell mediates Grave’s disease?

Answer 15

CD4 Th2 cells which cause excessive production and release of T3 and T4 thyroid hormone

Question 16

Someone with Grave’s disease will present with what signs/symptoms?

Answer 16

weight loss, heat intolerance, anxiety, irritability, exophthalmos

Question 17

What happens to the thyroid in grave’s disease?

Answer 17

The thyroid is destroyed by the body because it produces too much thyroid hormone

Question 18

How is Hashimoto’s disease different from Grave’s disease?

Answer 18

Hashimoto’s involves the destruction of normal thyroid tissue, whereas Grave’s disease involves the destruction of overstimulated thyroid

Question 19

Hypothyroidism occurs in what Type II AI disorder?

Answer 19

Hashimoto’s disease

Question 20

What cell mediates Hashimoto’s disease?

Answer 20

CD4 Th1 cells

Question 21

Because the thyroid is being attacked by the body, what distinct thing forms in the thyroid that can be used for diagnosis?

Answer 21

Ectopic lymphoid tissue

Question 22

What causes the enlarged thyroid in Hashimoto’s disease?

Answer 22

Ectopic lymphoid tissue

Question 23

What is Sjogren’s syndrome?

Answer 23

A progressive destruction of exocrine glands leading to low salivary levels

Question 24

Who is more likely to get Sjogren’s syndrome?

Answer 24

Women are 9x more likely to get it

Question 25

What three signs/symptoms should you expect to find in a Sjogren’s patient?

Answer 25

Dry eyes, dry mouth, arthritis

Question 26

What form in the ducts of salivary glands in Sjogren’s syndrome?

Answer 26

Periductal aggregates of antibodies and antigen

Question 27

What kind of hypersensitivity reaction is Sjogren’s Syndrome?

Answer 27

Type II hypersensitivity

Question 28

What mediates or causes Type III AI disorders?

Answer 28

IgG that binds to antigens in the blood or tissue, and then form an aggregate

Question 29

What causes Systemic Lupus Erythematosus (SLE)?

Answer 29

Self-antigen targeting and deposition of aggregates in the blood vessels