Immunology

Question 1

Provide possible sources of autoimmunity.

Answer 1

Escape of autoreactive T cells.
Activation of Self
Autoantibody Production
Expansion of pathogenic lineage
Failed regulation
Entry into tissues
Inflammation

Question 2

Describe type 2 autoimmunity.

Answer 2

Ab against cell-surface antigen or matrix Ag
binds:
-activates complement
-FcR, phagocytic, and NK cells

Self-Ag cell eliminated
Tissues (self-Ag) chronic inflammation
Ab- alter cellular function

Question 3

Describe AHA, in terms of type 2 hypersensitivity.

Answer 3

Self-Ag cell eliminated.
FcR in spleen
lysis

Question 4

Describe Goodpasture’s syndrome, in terms of type 2 hypersensitivity.

Answer 4

Tissue destruction
Ab– type 4 collagen- binds to basement membrane of renal glomeruli and pulmonary alveoli
Recognized by Fc receptors on macrophages and Nk cells
complement
sublytic membrane attack complexes (chronic inflammation)

Question 5

Describe Myasthenia Gravis, in terms of type 2 hypersensitivity.

Answer 5

Altered cell function
Ab- blocks acetylcholine receptor
downregulation of its receptor
decrease Na+ uptake,
receptor not triggered, muscle weakness

Question 6

What is the treatment of myasthenia gravis?

Answer 6

Pridostigmine
Plasmaphoresis

Question 7

Describe Graves Disease, in terms of type 2 hypersensitivity.

Answer 7

Altered cell function
Ab mimics the TSH receptor, and TSh binds to it
Stimulation of T3 and T4
Hyperthyroidism

Question 8

What is the treatment for graves disease?

Answer 8

Suppressed thyroid function
Thyroid ablation, surgery, and radioactive iodine
B cell depletion

Question 9

Describe type 3 Hypersensitive reaction.

Answer 9

Excess Ab-Ag complexes- clog the system and trigger inflammation
Large doses of Ag
The constant release of self-Ag
AB against ubiquitous Ag DNA

Leads to SLE,

Question 10

Which sites are usually involved in type 3 hypersensitivity?

Answer 10

Deposition Bloodvessels, Kidney, and skin

Question 11

Explain how clearance works.

Answer 11

Apoptotic cells cleared by macrophages and opsonins
This avoids exposure autoAg- promotes tolerance

Question 12

Explain what happens to tolerance in SLE

Answer 12

less effective clearance, AutoAg exposure- SNECs
release of proinflammatory cytokines
SNECS-Ab deposits in tissues and detected by circulating Mac and DC- release IFN a and inflammatory cytokines
INF is unabated- tissue damage and cell death
they accumulate GC, Ag to Follicular DC- Autoreactive B cells
Autoimmune is initiated

NETS
initiate antineutrophil cytoplasmic Ab.
internalization of ANCA-Ab by pDC
enhances IFNa- neutrophils primed to NETosis
DNase inhibitors, anti-dsDNA autoantibodies and low levels of opsonins in patients with SLE worsen the clearance of NETs

A vicious cycle is initiated leading to the formation and deposition of more IC, inflammation, cell death, and organ damage.

Question 13

Describe Corticosteroids as immunotherapy.

Answer 13

Alteration in gene transcription leads
decrease
prostaglandin synthesis
reduction of histamine and bradykinin release

Question 14

Which cell mediates Type 4 hypersensitivity?

Answer 14

T cell

Question 15

What is autoimmunity?

Answer 15

Immune response directed against self (auto-) antigens results in inflammation and destruction of healthy tissues.

Question 16

What is immunological tolerance?

Answer 16

Unresponsiveness to an antigen-induced by exposure of lymphocytes to that antigen; antigen-specific

Question 17

Describe risk-associated HLA-DR and HLA-DQ haplotypes.

Answer 17

Efficient presentation of autoimmunity-inducing peptides.

Question 18

Describe protective HLA-DR and HLA-DQ haplotypes.

Answer 18

Inability to present critical antigen epitopes to T helper cells and competition for binding with risk haplotypes.

This means that when those epitopes are presented on the surface of infected cells or antigen-presenting cells, they are more likely to bind to the receptors on the T helper cells that carry the risk haplotype.

Question 19

Describe risk-associated class 1 Allele.

Answer 19

Efficient presentation of critical antigen epitopes to cytotoxic CD8 T cells