Infectious disease Flashcards
characteristics of adaptive immune system (active)
- highly specific to Ag
- shows memory
- has cellular (cytotoxic/helper/memory t cells) & humoral component (plasma cells, b cells)
what is antigen presentation?
- APC like dendritic cells & macrophage
- engulf pathogen by phagocytosis
- process Ag
- present as peptide: MHC complex to native T cell
how does peptide: MHC form?
- lysosome contains hydrolytic enzymes that digest pathogens into small peptides
- at RER: peptide of Ag will bind to Major Histocompatibility Complex -> form peptide: MHC complex
- at GA: peptide: MHC complex transported to plasma membrane of APC via transport vesicles
- Ag of pathogen is now presented on plasma membrane of APC to naive T cells
how does peptide: MHC form?
- lysosome contains hydrolytic enzymes that digest pathogens into small peptides
- at RER: peptide of Ag will bind to Major Histocompatibility Complex -> form peptide: MHC complex
- at GA: peptide: MHC complex transported to plasma membrane of APC via transport vesicles
- Ag of pathogen is now presented on plasma membrane of APC to naive T cells
what is clonal selection?
- single B/T cell recognise an Ag that enters body
- is selected from pre-existing cell pool of differing Ag specificities
- then reproduce to generate clonal cell population that eliminate Ag
what is the process of T cell activation?
- each naive T cell has a specific T-cell receptor complementary C&C to peptide:MHC on APC & bind
- APC secretes cytokines
- activates specific naive T cell to undergo clonal expansion & differentiation into effector cytotoxic & helper T cells
what is the process of B cell presentation of peptide:MHC?
- naive B cell has specific BCR w/ ABS complementary C&C to Ag on pathogen
- cell membrane invaginates & pinches off, placing pathogen into endocytic vesicle via receptor-mediated endocytosis
- endocytic vesicle fuse with lysosome
- pathogen is digested into small peptides which combines with MHC protein to form peptide:MHC complex
- transported to CSM of naive B cell for presentation of specific T helper cell
what happens to cellular component after T cell differentiation?
- cytotoxic T cells kill intracellular infected cells
- through expressing same specific Ag of pathogen
- by releasing perforins (make pores on CSM) & granzymes (diffuse through pores into cytosol to activate enzymes involved in apoptosis)
what is the process of B cell activation?
- specific helper T cell w/ specific TCR bind to complementary peptide:MHC presented on specific naive B CSM
- helper T cell secrete cytokines to activate specific B cell
- resulting in CE & DyDx to form antibody-secreting plasma cells & memory B cells (humoral response)
what is CE & DyDx?
- repeated division of cells by mitosis
- specialisation of cells due to differential switching on of genes (form 2 types of cells: plasma+memory B)
what are the functions of antibodies? + (humoral response)
- neutralisation: ABS of antibodies bind to Ag -> prevent binding of pathogen to host cell receptor -> prevent cell entry
- agglutination: AB has 2 ABS -> bind to Ag of 2 pathogens simultaneously -> cause clumping of pathogen & promote phagocytosis
- opsonisation: Fc region of AB bind to Fc region on pathogen -> tags pathogen & promote phagocytosis
what is the function of hinge region of AB?
gives flexibility when binding to epitope of Ag
what is the function of disulfide bridges?
- hold heavy & light chain together
- stabilise quaternary structure
what is the constant region of heavy chan?
determines class & function of AB
what is the process of somatic recombination?
- random DNA rearrangement
- previously separated DNA sequences are randomly joined together
- (lg heavy chain gene locus): V + D + J segment randomly joined to form single VDJ exon
- (lg light chain gene locus): V + J segment randomly joined to form single VJ exon
when does somatic recombination occur?
- during B cell maturation in bone marrow
- from immature B cell to naive B cell
when does somatic hypermutation & class switching occur?
- after activation of B cell in lymph nodes
- from naive B cell to plasma cell
what is the process of somatic hypermutation?
- random point mutation in rearranged VDJ/VJ regions in activated B cells
- further diversifies variable regions for Ag binding
- occurs during clonal expansion of activated B cells
- result in B cells expressing lower/ higher affinity lg chains on their CSM
- B cells expressing higher affinity BCR on CSM are selected for CE & dydx
- resultant B cells, plasma cells & hence AB have higher affinity ABS for specific Ag
what comprises of innate immune system? (passive)
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
what comprises of adaptive immunity?
[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
how does immunological memory come about?
- rapid re-introduction of Ag-specific AB
- protect against re-infection
- due to memory B & T cells staying for very long
- long-term protection
EG) VACC: active, artificial
compare primary vs secondary immune response
- no lag period (naive T and B no need to be activated -> due to pool of memory T & B
- faster (reactivate easily -> fast increase in AB)
- stronger (AB increase quickly & peak higher)
- high AB persist over longer time
what is vaccination?
- intentional administration of harmless form of pathogen
- to induce specific adaptive immune system
- protects individuals against later exposure to pathogen
- due to production of memory B & T cells
- a form of active, artificial immunity
how does antibiotic resistance build up?
- failure to complete course of antibiotics
- some bacteria survive
- spontaneous mutation in bacterial population produce AR strains
- transfer of AR genes from bacterium to bacterium via C/T/T
- when antibiotics is given, it acts as selection PA
- those w/ AR gene will survive, reproduce & pass on alleles to daughter cells but those susceptible will die
- over few generations-> microevo
- increase freq. of AR alleles in population
