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H2 Biology > Infectious disease > Flashcards

Infectious disease Flashcards

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1
Q

characteristics of adaptive immune system (active)

A
  1. highly specific to Ag
  2. shows memory
  3. has cellular (cytotoxic/helper/memory t cells) & humoral component (plasma cells, b cells)
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2
Q

what is antigen presentation?

A
  1. APC like dendritic cells & macrophage
  2. engulf pathogen by phagocytosis
  3. process Ag
  4. present as peptide: MHC complex to native T cell
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3
Q

how does peptide: MHC form?

A
  1. lysosome contains hydrolytic enzymes that digest pathogens into small peptides
  2. at RER: peptide of Ag will bind to Major Histocompatibility Complex -> form peptide: MHC complex
  3. at GA: peptide: MHC complex transported to plasma membrane of APC via transport vesicles
  4. Ag of pathogen is now presented on plasma membrane of APC to naive T cells
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4
Q

how does peptide: MHC form?

A
  1. lysosome contains hydrolytic enzymes that digest pathogens into small peptides
  2. at RER: peptide of Ag will bind to Major Histocompatibility Complex -> form peptide: MHC complex
  3. at GA: peptide: MHC complex transported to plasma membrane of APC via transport vesicles
  4. Ag of pathogen is now presented on plasma membrane of APC to naive T cells
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5
Q

what is clonal selection?

A
  1. single B/T cell recognise an Ag that enters body
  2. is selected from pre-existing cell pool of differing Ag specificities
  3. then reproduce to generate clonal cell population that eliminate Ag
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6
Q

what is the process of T cell activation?

A
  1. each naive T cell has a specific T-cell receptor complementary C&C to peptide:MHC on APC & bind
  2. APC secretes cytokines
  3. activates specific naive T cell to undergo clonal expansion & differentiation into effector cytotoxic & helper T cells
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7
Q

what is the process of B cell presentation of peptide:MHC?

A
  1. naive B cell has specific BCR w/ ABS complementary C&C to Ag on pathogen
  2. cell membrane invaginates & pinches off, placing pathogen into endocytic vesicle via receptor-mediated endocytosis
  3. endocytic vesicle fuse with lysosome
  4. pathogen is digested into small peptides which combines with MHC protein to form peptide:MHC complex
  5. transported to CSM of naive B cell for presentation of specific T helper cell
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8
Q

what happens to cellular component after T cell differentiation?

A
  1. cytotoxic T cells kill intracellular infected cells
  2. through expressing same specific Ag of pathogen
  3. by releasing perforins (make pores on CSM) & granzymes (diffuse through pores into cytosol to activate enzymes involved in apoptosis)
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9
Q

what is the process of B cell activation?

A
  1. specific helper T cell w/ specific TCR bind to complementary peptide:MHC presented on specific naive B CSM
  2. helper T cell secrete cytokines to activate specific B cell
  3. resulting in CE & DyDx to form antibody-secreting plasma cells & memory B cells (humoral response)
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10
Q

what is CE & DyDx?

A
  1. repeated division of cells by mitosis
  2. specialisation of cells due to differential switching on of genes (form 2 types of cells: plasma+memory B)
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11
Q

what are the functions of antibodies? + (humoral response)

A
  1. neutralisation: ABS of antibodies bind to Ag -> prevent binding of pathogen to host cell receptor -> prevent cell entry
  2. agglutination: AB has 2 ABS -> bind to Ag of 2 pathogens simultaneously -> cause clumping of pathogen & promote phagocytosis
  3. opsonisation: Fc region of AB bind to Fc region on pathogen -> tags pathogen & promote phagocytosis
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12
Q

what is the function of hinge region of AB?

A

gives flexibility when binding to epitope of Ag

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13
Q

what is the function of disulfide bridges?

A
  1. hold heavy & light chain together
  2. stabilise quaternary structure
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14
Q

what is the constant region of heavy chan?

A

determines class & function of AB

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15
Q

what is the process of somatic recombination?

A
  1. random DNA rearrangement
  2. previously separated DNA sequences are randomly joined together
  3. (lg heavy chain gene locus): V + D + J segment randomly joined to form single VDJ exon
  4. (lg light chain gene locus): V + J segment randomly joined to form single VJ exon
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16
Q

when does somatic recombination occur?

A
  1. during B cell maturation in bone marrow
  2. from immature B cell to naive B cell
17
Q

when does somatic hypermutation & class switching occur?

A
  1. after activation of B cell in lymph nodes
  2. from naive B cell to plasma cell
18
Q

what is the process of somatic hypermutation?

A
  1. random point mutation in rearranged VDJ/VJ regions in activated B cells
  2. further diversifies variable regions for Ag binding
  3. occurs during clonal expansion of activated B cells
  4. result in B cells expressing lower/ higher affinity lg chains on their CSM
  5. B cells expressing higher affinity BCR on CSM are selected for CE & dydx
  6. resultant B cells, plasma cells & hence AB have higher affinity ABS for specific Ag
19
Q

what comprises of innate immune system? (passive)

A

1st line: physical & chemical barrier
- skin & mucosa prevent entry of pathogens
- lysozyme: hydrolysis peptidoglycan cell wall
- acidic pH in stomach kills most pathogen

2nd line: cellular component
- natural killer T cells: kill defective cells
- dendritic cells + macrophage (phagocytosis): APC
- neutrophils: phagocytosis of pathogen & toxin

3rd line: inflammation
- macrophage induce inflammation by secreting cytokines & chemokines
- lead to vasodilation, fluid accumulation & attract neutrophils

phagocytosis
- macrophage form pseudopodia to engulf pathogen
- form phagosome
- fuse with lysosome
- enzymes in lysosome digest pathogen

20
Q

what comprises of adaptive immunity?

A

[active]
1. natural: infected by pathogen
2. artificial: memory cell production -> vacc

[passive]
1. natural: antibodies from mum via placenta/breastmilk
2. artificial: antiserum w/ AB from another host

21
Q

how does immunological memory come about?

A
  1. rapid re-introduction of Ag-specific AB
  2. protect against re-infection
  3. due to memory B & T cells staying for very long
  4. long-term protection
    EG) VACC: active, artificial
22
Q

compare primary vs secondary immune response

A
  1. no lag period (naive T and B no need to be activated -> due to pool of memory T & B
  2. faster (reactivate easily -> fast increase in AB)
  3. stronger (AB increase quickly & peak higher)
  4. high AB persist over longer time
23
Q

what is vaccination?

A
  1. intentional administration of harmless form of pathogen
  2. to induce specific adaptive immune system
  3. protects individuals against later exposure to pathogen
  4. due to production of memory B & T cells
  5. a form of active, artificial immunity
24
Q

how does antibiotic resistance build up?

A
  1. failure to complete course of antibiotics
  2. some bacteria survive
  3. spontaneous mutation in bacterial population produce AR strains
  4. transfer of AR genes from bacterium to bacterium via C/T/T
  5. when antibiotics is given, it acts as selection PA
  6. those w/ AR gene will survive, reproduce & pass on alleles to daughter cells but those susceptible will die
  7. over few generations-> microevo
  8. increase freq. of AR alleles in population

H2 Biology (19 decks)

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