W13L22 - Immune Response to Infectious Diseases Flashcards
Immunity to Fungi
Depends on identity - virulence factors - physiological traits - nutritional requirements Immunosuppression is most important predisposing patient factor Innate - phagocytosis - neutrophils - macrophages Acquired - cell mediated immunity - extracellular fungi - Th17 response - intracellular fungi - macrophage response with Th1
IR to Fungi - Cytokine Release
Both innate and adaptive IR to gundi results in cytokine release
IL-17 recruits neutrophils
Both IL-17 and Il-22 stimulates release of antimicrobial peptides
Immune Response to Viruses
Innate and adaptive responses to viruses aimed at blocking virus entry to cells and eliminating infected cells
Immune Response to Viruses - Innate Immunity
Inhibition of infection by type 1 interferons
- type 1 IFNs produced by virally infected cells
- they cause sequestration of lymphocytes to lymph nodes
- increase cytotoxicity of NJ cells
- type 1 IFNs can prime nearby uninfected cells as well as being self acting on an infected cell
- can stimulate internal mechanisms for inhibiting progression of viral infection in uninfected cells
Internal Mechanisms of Type 1 IFN
- Inhibit viral protein synthesis in infected cells
- Stimulates production of enzymes which can degrade viral RNA
- Can inhibit viral gene expression and viron assembly
Mechanisms for Removing Tumor/Virus Cells
- NK cells (innate IR) kill by detecting lack of MHC class 1 on cell surface
- NK cells (adaptive) kill by detecting antibody bound to a cell
- Cytotoxic (adaptive) T cells kill by detecting antigen presented on MHC 1
Immune Response to Viruses - Adaptive Immunity
Type 1 IFNs
- increase cytotoxicity of CD8+ cytotoxic lymphocytes
- promotes differentiation of naive T cells into Th1 cells
- up regulates expression of class 1 MHC molecules on the surface of infected cells
Killing of infected cells by CD8+ cytotoxic lymphocytes
Antibody dependent cell mediated cytotoxicity
Neutralisation of virus particles by antibody
Virus Adaptive Immunity - CD8+ Cytotoxic Lymphocytes
APCs phagocytose viral infected host cells
APCs present viral antigens to primed Th1 cells and naive cytotoxic T cells
Th1 cells release IFNγ and IL2
Cytotoxic T cells become primed to recognise virally infected cells
Virus Adaptive Immunity - Antibody Dependent Cell-Mediated Cytotoxicity
NK cells detect antibody coated cells via Fc receptors
Mechanism for removal of tumor cells and virally infected cells
Antibody isotope only IgG (Th1)
Virus Adaptive Immunity - Neutralisation of Viruses by Abs
Abs bind to surface antigens of a virus particle
Blocks adhesion of virus to mucosal epithelium/cell membrane
Antibody isotopes - IgG1 and 3 (Th1), IgA (Th2), IgM (still adaptive but no Th1 or 2 required)
Then targeted by NK cells and phagocytes
Why can viruses still cause illness?
Antigenic variation Inhbition of presentation of MHC class 1 IL1 normally promotes inflammation IFNγ normally promotes: - Th1 differentiation - B cell isotope switching to IgG - activation of macrophages (Th1) - increased expression of class 1 and 2 MHC IL10 inhibits IL12
Antigenic Shift and Antigenic Drift
Antigenic shift - genetic re-assortment of genes - creates new viruses - antigenically distinct precursors Antigenic Drift - mechanism of variation in viruses by mutation - accumulation of mutations in genes that encode for surface antigens - occurs in influenza A
Immune Response to Parasites
Innate
- phagocytosis by macrophages/neutrophils
- many protozoa can survive inside phagocytes
Adaptive
- protozoa: Th1 assisted phagocytosis (IFNγ) and CD8 cytotoxic T cells
- helminths: Th2 and IgE leading to activated eosinophils