Immunology - Autoimmune

Front 1

Myasthenia Gravis

-mediator
-antigen
-result

Back 1

Mediator: antibody

Antigen: acetylcholine receptor

Result: muscle weakness

Front 2

Sjogrens Syndrome

-mediator
-antigen
-result

Back 2

Mediator: antibody, T-cell

Antigen: secretory duct

Result: lymphocyte infiltration of exocrine gland; dry mouth and dry eyes

Front 3

Systemic Lupus Erythematosus (SLE)

-mediator
-antigen
-result

Back 3

Mediator: antibody, T-cell

Antigen: DNA, histones, RNA proteins

Result: glomerulonephritis, arthritis, vasculitis, rash

Front 4

Multiple Sclerosis

-mediator
-hypersensitivity 'type'
-antigen
-result

Back 4

Mediator: T-cell

Hypersensitivity: Type IV

Antigen: myelin basic protein

Result: demyelination, sclerotic plaques

Front 5

Type-1 Diabetes Mellitus

-mediator
-hypersensitivity 'type'
-antigen
-result

Back 5

Mediator: T-cell

Antigen: pancreatic beta-cell antigen

Hypersensitivity: Type IV

Result: destruction of beta-cells; insulin deficiency

Front 6

Hashimoto's Thyroiditis

-mediator
-antigen
-result

Back 6

Mediator: antibody, T-cell

Antigen: thyroid antigens

Result: thyroid tissue breakdown, which leads to hypothyroidism

Front 7

Rheumatoid Arthritis (RA)

-mediator
-hypersensitivity 'type'
-antigen
-result

Back 7

Mediator: antibody, T-cell

Hypersensitivity: Type III + Type IV

Antigen: IgG (complexes w/ RF), unknown joint synovium antigens, platelet-derived microvesicles

Result: joint inflammation, destruction

Front 8

Grave's Disease

-mediator
-antigen
-result

Back 8

Mediator: antibody

Antigen: thyroid-stimulating-hormone receptor

Result: hyperthyroidism

Front 9

Autoimmune Hemolytic Anemia

-mediator
-hypersensitivity 'type'
-antigen
-result

Back 9

Mediator: antibody

Hypersensitivity: Type II

Antigen: Rh blood group (on RBC surface)

Result: RBC destruction, anemia

Front 10

Goodpasture's Syndrome

-mediator
-hypersensitivity 'type'
-antigen
-result

Back 10

Mediator: unknown

Hypersensitivity: Type II

Antigen: collagen type-IV

Result: glomerulonephritis, pulmonary hemorrhage

Front 11

Acute Rheumatic Fever

-mediator
-hypersensitivity 'type'
-antigen
-result

Back 11

Mediator: antibody, T-cell

Hypersensitivity: Type II

Antigen: heart muscle

Result: myocarditis, arthritis, scarring of heart valve

Front 12

Mixed Essential Cryoglobulinemia

-mediator
-hypersensitivity 'type'
-antigen
-result

Back 12

Mediator: antibody (rheumatoid factor - IgM)

Hypersensitivity: Type III

Antigen: IgG

Result: systemic vasculitis

Front 13

Five diseases that can cross the placenta are:

Back 13

1. Myasthenia gravis
2. Graves' disease
3. Thrombocytopenic purpura
4. Neonatal lupus rash -- Congenital heart block
5. Pemphigus vulgaris

Front 14

Five "systemic" autoimmune diseases are:

Back 14

1. RA (rheumatoid arthritis)
2. Scleroderma
3. Lupus
4. Sjogren's syndrome
5. Polymyositis

Front 15

Nine "organ-specific" autoimmune diseases are:

Back 15

1. Type-1 DM
2. Goodpasture's
3. Multiple sclerosis
4. Graves'
5. Hashimoto's thyroiditis
6. Autoimmune hemolytic anemia
7. Addison's disease
8. Vitiligo
9. Myasthenia gravis

Front 16

Which disease is characterized by anti-adrenal tissue Abs

Back 16

Addison's disease

Front 17

Which disease is characterized by anti-melanin production.

Back 17

Vitiligo

Front 18

Which disease is characterized by anti-muscle tissue Abs

Back 18

Polymyositis

Front 19

Thrombocytopenic purpura

-mediator
-hypersensitivity 'type'
-antigen

Back 19

Mediator: antibody

Hypersensitivity: Type II

Antigen: platelet integrin

Result: abnormal bleeding

Front 20

This type of immune response is defined as:
Antibody against cell-surface or extracellular matrix proteins

Back 20

Type II

Front 21

This type of immune response is defined by:
Immune complex formation

Back 21

Type III

Front 22

This type of immune response is defined as:
T-cell mediated

Back 22

Type IV

Front 23

RBC's coated with IgG autoantibody are cleared from the body by:

Back 23

FcR+ macrophages

Front 24

Intravascular hemolysis of RBC's is caused by:

Back 24

The binding of autoantibodies that fix complement and the formation of MAC (Membrane Attack Complex)

Front 25

Graves' disease disrupts feedback regulation and causes hyperthyroidism by:

Back 25

*Anti-TSH-receptor Ab acts as a TSH-receptor agonist
*When thyroid hormone signals the pituitary to stop secreting TSH, the anti-TSH-r Ab continues to stimulate thyroid hormone secretion

Front 26

When auto-Abs bind muscle ACh receptors, the receptors are internalized and degraded. The decreasing number of ACh receptors results in unresponsive muscle.
This disease is called:

Back 26

Myasthenia gravis

Front 27

Type-2 Diabetes

-mediator
-hypersensitivity 'type'
-antigen
-result

Back 27

Mediator: antibody (acts as antagonist)

Hypersensitivity: Type II

Antigen: Insulin receptor

Result: hyperglycemia, ketoacidosis

Front 28

Hypoglycemia

-mediator
-hypersensitivity 'type'
-antigen
-result

Back 28

Mediator: antibody (acts as agonist)

Hypersensitivity: Type II

Antigen: Insulin receptor

Result: hypoglycemia

Front 29

Auto-Abs in Goodpasture's disease react with basement membrane of which 2 locations of the body?

Back 29

1. Glomerulus

2. Lungs

Front 30

This disease is caused by anti-nuclear IgG. A large amount of small immune complexes are formed and deposited in small blood vessels of the renal glomerulus.

Back 30

SLE - Systemic Lupus Erythematosus

Front 31

How is autoimmune-related tissue damage "self-perpetuating"

Back 31

Upon cell death, self antigens are released. B-cell recognizes self-antigen and is activated by a T-cell. B-cell releases auto-Ab that initiates inflammatory response. More cells are injured as a result, and more self antigen is released

Front 32

When B-cells specific for various components of a complex antigen are stimulated by a self-reactive T-helper cell of a single specificity...
This phenomenon is called:

Back 32

"epitope spreading"

Front 33

Explain the process of Multiple Sclerosis

Back 33

1. Blood Brain Barrier becomes permeable to leukocytes and blood proteins.

2. activated T-cells encounter self CNS antigen presented on MHC-II of microglial cells

3. Inflammatory reaction occurs due to mast-cell activation, complement, Abs and cytokines

4. anti-MBP (myelin basic protein) Abs cause demyelination

Front 34

Explain the process of Rheumatoid Arthritis

Back 34

1. Lymphocyte + Macrophage Recruitment
2. Macrophage Activation and Cytokine Release
3. Osteoclast Activation
4. Bone + Joint Destruction

1. inflammation of synovial membrane attracts self-reactive lymphocytes and macrophages
2. self-reactive CD4 T-cells activate macrophages, which secrete cytokines
3. cytokines activate bone-destroying osteoclasts
4. osteoclasts destroy joints

Front 35

For each disease, which is the pathogenic effector, T-cells or Abs:

-Lupus
-Type 1 DM
-Myasthenia gravis
-Mult. sclerosis

Back 35

Lupus: Abs
Type 1 DM: T-cells
Myasthenia gravis: Abs
Mult. sclerosis: T-cells

Front 36

4 immunologically privileged sites:

Back 36

1. Brain
2. Eye
3. Testis
4. Uterus

Front 37

Immunologically privileged sites:
- 3 main characteristics

Back 37

1. aren't drained by lymphatics
2. contain sequestered antigen
3. contain immunosuppressive environment (Ag is recognized but ignored)

Front 38

Describe: Sympathetic Ophthalmia

Back 38

Upon injury, sequestered Ag of the eye (privileged site) is released and carried to lymph nodes.
T-cells are activated and travel to site of injury

Front 39

nearly all type-1 diabetic individuals express which allele, or alleles, of the HLA gene?

Back 39

DR3, DR4 or both DR3 + DR4

Front 40

the majority of type-1 diabetic individuals do NOT express which allele of the HLA gene?

Back 40

DR2

Front 41

What external events can initiate autoimmunity

Back 41

1. Inocuous viral infections
2. Molecular mimicry
3. Drugs + Toxins

Front 42

Define Molecular Mimicry

Back 42

molecular mimicry: occurs when pathogens express surface molecules that mimic host molecules, resulting in cross-reactive Abs

Front 43

Autoimmune diseases that can cross the placenta are mediated by which immunoglobulin?

Back 43

IgG

Front 44

T-reg cells secrete _____ and _____ to suppress self-reactive T-cells

Back 44

IL-10
TGF-Beta

Front 45

"tolerance" developed by lymphocytes shortly after it starts to express its Ag-receptor.

Back 45

Central tolerance

Front 46

"tolerance" induced in mature lymphocytes repertoire AFTER leaving central lymphoid organs

Back 46

Peripheral tolerance

Front 47

3 principle mechanisms of Peripheral Tolerance:

Back 47

1. anergy
2. clonal deletion
3. suppression via T-reg cells

Front 48

Name the 6 layers, or mechanisms, of self-tolerance:

Back 48

1. central tolerance
2. antigen segregation
3. peripheral anergy
4. regulatory cells
5. cytokine deviation
6. clonal deletion

Front 49

Explain "peripheral anergy"

Back 49

cellular inactivation due to a lack of sufficient signaling

Front 50

Explain "cytokine deviation"

Back 50

differentiation to T-h2 cells limits inflammatory cytokine production

Front 51

Explain "clonal deletion"

Back 51

post-activation apoptosis

Front 52

Explain "central tolerance"

Back 52

* pre-activation apoptosis
* TCR editing

Front 53

The 2 MOST COMMON autoimmune diseases are:

Back 53

thyroiditis and rheumatoid arthritis

Front 54

the "autoimmune regulator" gene is:

Back 54

the gene that expresses tissue-specific antigens in the thymus, where T-cells mature

Front 55

"Rheumatoid factor" is:

Back 55

anti-IgG IgM

Front 56

these T-cells:
-recognize MHC-I:peptide ligands
-express CD8 surface protein

Back 56

CTL's or Tc-cells

Front 57

these T-cells:
-recognize MHC-II:peptide ligands
-express CD4 surface protein

Back 57

T-helper cells