Immune Response To Microbial Infections Flashcards
Host Pathogen Interactions and what decides if infection will occur
Transmission and entry—> Colonization—> multiplication—>invasion of host tissue—>dissemination—> damage to the host cells
Pathogen virulence factors (Host immune status)
General features of Immune response against pathogens
Innate and adaptive
Distinct and specialized immune response for different microbes
Evade immune mechanisms
Latent or persistent infections
Different Types of microbes
Parasites protozoa etc
Extracellular parthogens: can grow and reproduce freely and move extensively in tissues caught by antibodies complement immune cells
Intracellular Pathogens: Can live inside host cells Hide from antibodies complement etc Navigate the intracellular immune response
Which part of the immune system provides a distinct and specialized immune responses for different types of microbes? Mediators of adaptive immune system
Adaptive
CD4 T cells Th1 Th2 and Th17
CD8 Tcells
Antibodies - different isotypes
CD4 T cell
Th1–> IL12–> IFN g macrophages
Th2–> IL4–> IL4, IL5, IL13 eosinophil helminths
Th17–> IL1, IL6, IL23 TGFB—> IL17 IL22–> Neutrophils—> extracellular bacteria and fungi
CD8 T cells and Antoibody Isotopes
Antigen recogn and conjugate formation—> CTL activation—> Granule exocytosis—> Detachment of CTL—> Target cell death
CD40 - CD40L and cytokines required for class switching
Cytokines involved IL4 —> IgE immunity against helminths type 1 hypersensitity and IgA mucosal
Mucosal tissues cytokines—> TGFB BAFF—> IgA—> mucosal immunity through breast milk
IgG Subclasses —> Opsonization complement activation neonatal immunity
Extracellular bacteria: strep psueu, neisseria spp and staph aur
Capable of replicating outside host cells; replicate through blood, CT, airway, GI tract
Innate immune components: Complement and neutrophils
Adaptive immune components: Antibodies (humoral immunity) and Th17 cells
Which Innate immune mediator may be important in killing extracellular bacteria?
Complement
GPB - Peptidoglycan and GNB - LPS - activate alternative pathway Mannose on bacteria surface - lectin pathway
Phagocytosis by neutrophils & macrophages
Phagocytes & complement—> cytokines—> leukocyte infiltration—> destroy bacteria
Which adaptive immune mediator may be important in eliminating extracellular bacteria in blood
Antibodies mediate killing via neutralization—> opsonization and phagocytosis—> complement by classical pathway
Evasion Mechanism of Extracellular bacteria
Inhibition of complement activation; sialic acid deposition on surface
Defense against antibodies; antigenic variation, IgA protease
Resistance to phagocytosis; CAPSULAR POLYSACCHARIDE strep peu & Hae infl
ROS
Intracellular Bacteria; Innate immune cells that are involved during intracell bact infection?
Innate Immune response;
Macrophages—> IL12–> Th1–> NK cells
NK Cells (provides early defense) —> IFN g —> macrophages
Intracellular bacteria—> NK cells
What Happens when Mycobacterium Tuberculosis cannot be cleared by Macrophages?
Granuloma Formation around foci of infection
Alveolar macrophages produce TNF a, IL12/IFN gamma
MTB components activates TNF a —> disease progression and symptoms
Th1 type response and IFNy production; increase phogolytic, phagocytic, NO, cytokine production recruit more T and NK cells
What type of hypersensitivity do granulomas display?
Activation of NK cells
Type IV/delayed type hypersensitivity formed by macrophages and lymphocytes (T cells)
2 receptors:
a) Activation receptors; antibody coated cells, viral HA, lectins antigens searched for by NK cells on MHC I
B) Inhibitory Receptors; recognize MHC I on cells
MHC I expression when down-regulated by viral infections and tumor cells is marked by NK cells
Adaptive Immune Response
Would CD8 T cells play a role during intracellular bacteria infection?
Evasion mechanism of Intracellular Bacteria
Which adaptive immune system will kill if pathogen escape into the cytoplasm
Th1 response
Macrophage activation—> IL12–> Th1 —> IFN y
Yes
Inhibition of phagolysosome formation; Mycobacterium tuber and legionella
Inactivate ROS; Mycobacterium leprae
Destruction of phagosome membrane, escape into cytoplasm; listeria Monocytogenes
CD8 T cells
TB skin test develops an indurated erythematous lesion at injection site 3 days following injection of TB antigens
Mononuclear cell infiltration following chemokine release from memory CD4 cells