Immunity to Infectious Disease Flashcards
The innate immune system includes
- Anatomical barriers against infection (physical and chemical)
- Cellular responses
Entry point and immune tools
- The entry site and location of an infectious agent will determine which immune tools are available and best suited for pathogen detection and elimination
Mucosal are controlled by
Th2
Tetanus (extracellular)
- Th17 cells
- IgM
- IgG
- phagocytic cells
- neutrophils
- macrophages
- neutralization
- opsonization
Mucosal Pathogens (intracellular bacteria)
- MALT B and T cells
- Mast cells with IgE
- IgA neutralize pathogen by binding and inhibiting surface attachment
- macrophages
- complement
- IL-13, IL-4, and IL-5
IL-13
induces epithelial cell repair and mucus
IL-5
activates and recruits eosinophils
IL-4 and IL-13
recruit and activate M2 macrophages
Extracellular Pathogens are derives from
Tfh, Th17 and Th2
Extracellular Pathogens
- B cells
- IgG
- IgM
- Phagocytic cells
- Antimicrobial componuds
- Complement
IL-17
induce the production of antimicrobial peptides by epithelial cells
Intracellular pathogen requires a strong
Th1 pathway response
Intracellular pathogens
- when pathogen is in intracellular vesicles, activates PRRs and certain TLRs
FasL
induce apoptosis of bacteria-laden macrophages
IL-2
acts on naive CD4 and CD8 T cells
IL-3
Production of monocytes
TNF-a
Acts on local blood vessels
The response by the immune system to a pathogen is determines by
- the nature of the pathogen
2. the environment in which the pathogen is encountered
Viruses enter
through a cell surface receptor
Viruses once they get inside the cell
- replication can occur
- Error prone, leading to mutations
- influenza
During viral replication
- trigger humoral and cell mediated adaptive immunity mechanisms
Antiviral immunity
- prevented by physical and chemical barriers
- if penetrated, intrinsic or innate defenses come into play
- in order to clear viral infection that escape innate defenses, the acquired/adaptive immune defenses are activated
Viral infections: Innate immune response
- Complement, antimicrobial peptides, recognition of PAMPs
- PRRs induce type 1 interferon
- Type 1 interferons bind to IFN receptors and activate antiviral activity
Viral infection: Humoral immunity
- Antibody protection can foster opsonization, complement activation, phagocytosis
- Ab can’t target cells where viral genomes have integrated into host cell chromosomes
Viral Infection: Cell-mediated
- CD4+ helper T cells secrete cytokines that promote antiviral activity
- IFN-g directly induces an antiviral state in adjacent cells
- IL-2 indirectly assists via promotion of CTL differentiation
- CD8+ CTLs actively find and destroy virally infected host cells
Immune Evasion Strategies by virus
- Rapid mutation
- Latency and molecular mimicry
- inactivating cytokine signals
- inactivating immune cells
- blocking cellular pathways
- Viruses employ several different strategies to evade host defense mechanism
Hepatits C
overcomes interferon antiviral effects by blocking/inhibiting PKR
HSV
inhibits TAP activity effectively shutting down MHC class I presentation to CD8+ T cells
Measles virus/ HIV
inhibit MHC class II expression and presentation to helper T cells
EBV and HIV
Can cause immunosuppresion
Influenza and HIV
constantly change their surface Ag
Immunity to extracellular bacteria
- Ab provers effective mechanisms for elimination
Immunity for intracellular bacteria
Ab aren’t as affected
- Can activate NK cells and macrophages for clearance
- Ultimate effect is Th1-type DTH response
Immune evasions strategies by bacteria
- attachment to host cell
- proliferation
- invasion of host tissue
- toxin-induced damage to host cells
Parasitic infections
- account for enormous disease burden worldwide, especially in developing countries
- protozoans and metazoans
- complicated life cycle of parasites
Malaria
- Life cycle moves through liver/ RBCs
- Maturational changed allow Ag shifting
- intracellular phases resist Ab-based responses
- short blood circulation time of free parasite stage prevents effective immune stimulation
African sleeping sickness
- Moves from blood to central nervous system
- caused by two trypanosome species transmitted by tsetse fly bites
- protozoans differentiates and divides every 6 hours in blood
Leichmaniasis
- Lives in macrophage phagosomes
- localized cutaneous self-resolving lesion
- systemic visceral leishmaniasis
- resistance is mediated by an effective Th1 response and IFN-g secretion
Metazoan parasites
- Helminths
- ## Dont replicate in host