BIOL 435 Immunoparasitology and Hypersensitivities

Question 1

host immune response

Answer 1

-agent of NS on parasites
>they must evade it
*coevolutionary arms race

Question 2

evasion of immunity by parasites

Answer 2

1. Antigenic variation
2. Molecular mimicry
3. Immunosuppression

Question 3

Trypanosoma

Answer 3

-start to outweigh blood cells by massive replication
-transmitted via tsete fly
-variant surface glycoproteins
>period waves

Question 4

Leishmania

Answer 4

• infects and reproduces IN human macrophages
• transmission by sand fly vector
• ex. Leishmanis mexicana

Question 5

Leishmania mexicana

Answer 5

-causative agent of cutaneous lesions
-lesion capacity for self-healing over time
-parasite is more pathogenic when lesions occur in ear cartilage (pinna)
>limmited due to poor vascularization
>treatment and recovery more problematic

Question 6

Schistosoma

Answer 6

• cercariae released by snail into water
• evolved molecular mimicry
• coat external surface with host molecules to disguise
• also contains enzyme that will destroy host complement molecules

Question 7

immunological trade off

Answer 7

• protection via immunity-mediated parasite death and severe tissue damage
  eg. human schistosomes: formation of anti-egg granulomas in liver and spleen

Question 8

‘anti-eggs’

Answer 8

• eggs surrounded by T-cells and macrophages
• severe tissue damage over host’s life-time
• potential for parasite-induced mortality due to immunopathology
• constant exposure is the problem: hypersensitive inflammatory reaction

Question 9

hypersensitivity classes

Answer 9

1. Type I: allergy and atopy
2. Type II: Ab-mediated hypersensitivity
3. Type III: Immune complex-mediated hypersensitivity
4. Type IV: delayed type hypersensitivity (DTH)

Question 10

Type I

Answer 10

-IgE
-soluble Ag
ex. local and systemic anaphylaxis
>food and drug allergies

Question 11

Type I mechanism

Answer 11

• allergen-specific IgE bind to mast cells via their Fc receptor
• when specific allergen binds to IgE, cross-linking of IgE induces degranulation of mast cells

Question 12

Type II

Answer 12

-IgG or IgM
-cell-bound Ag
ex. RBC destruction after mismatched blood
>Rh- mom
>hemolytic anemia

Question 13

Type II mechanism

Answer 13

• IgG or IgM binds to cellular Ag, leading to C’ activation and cell lysis
• IgG can also mediate ADCC with CTL, macrophages and neutrophils

Question 14

IgG, IgM kills cells in 3 ways

Answer 14

1. Activate complement (ex. MAC)
2. ADCC
3. Ab (can be opsonin)

Question 15

Type III

Answer 15

-IgG and IgM
-soluble Ag
ex. rheumatoid arthritis
>systmic lupus

Question 16

Type III mechanism

Answer 16

• Ag-Ab complexes are deposited in tissues
• C’ activation provides inflammatory mediators and recurits neutrophils
• enzymes released from neutrophils damage tissue

Question 17

Type IV

Answer 17

-T-cells
-soluble or cell-bound Ag
-ex. type I diabetes mellitus
>MS

Question 18

Type IV mechanism

Answer 18

-Th1 cells secrete cytokines, which activate macrophages and CTL
1. Sensitization
2. Immune response
>influx of cytokines and CTLs, build up enzymes which cause tissue damage