Pattern Recognition Receptors (PRRs) in Immune Response

Pattern Recognition Receptors (PRRs)

• Types:
  • Toll-like receptors (TLRs)
  • NOD-like receptors (NLRs)
  • RIG-I-like receptors (RLRs)
  • C-type lectin receptors (CLRs)
• Function:
  • Recognize pathogen-associated molecular patterns (PAMPs)
  • Activate immune response through signaling pathways
  • Trigger production of pro-inflammatory cytokines and type I interferons
• Examples:
  • TLR4 recognizes LPS from Gram-negative bacteria
  • TLR2 recognizes lipoteichoic acid from Gram-positive bacteria
  • NOD2 recognizes muramyl dipeptide from bacterial peptidoglycan

Complement System

• A group of proteins that work together to:
  • Mark pathogens for destruction
  • Activate immune cells
  • Inflame tissues
• Three main pathways:
  • Classical pathway: activated by antibody-bound pathogens
  • Alternative pathway: activated by pathogens without antibody
  • Lectin pathway: activated by mannose-binding lectin
• Key components:
  • C3 (central component)
  • C5-9 (membrane attack complex)
  • C1q, C4, C2 (classical pathway)
  • Factor B, Factor D (alternative pathway)
• Functions:
  • Opsonization: marking pathogens for phagocytosis
  • Chemotaxis: attracting immune cells to site of infection
  • Cytolysis: direct killing of pathogens

Neutrophil Function

• Key functions:
  • Phagocytosis: engulfing and digesting pathogens
  • Degranulation: releasing enzymes and antimicrobial granules
  • Respiratory burst: producing reactive oxygen species (ROS)
• Mechanisms:
  • Recognition of pathogens through PRRs and Fc receptors
  • Activation of NADPH oxidase for ROS production
  • Release of granules containing enzymes (e.g., elastase, myeloperoxidase)
• Importance:
  • First line of defense against bacterial infections
  • Rapid response to tissue damage and inflammation

Natural Killer Cell Biology

• Characteristics:
  • Large granular lymphocytes
  • No antigen-specific receptor
  • Spontaneous cytotoxicity against tumor cells and virally infected cells
• Activation:
  • Through recognition of missing or altered self-MHC molecules
  • Via activating receptors (e.g., NKp46, NKp30, NKG2D)
  • By cytokines (e.g., IL-2, IL-12, IL-15)
• Functions:
  • Direct cytotoxicity: killing target cells through granzyme and perforin
  • Cytokine production: IFN-γ, TNF-α, and others
  • Modulation of immune response: regulating T cell and dendritic cell activity

Pattern Recognition Receptors (PRRs)

• Recognize pathogen-associated molecular patterns (PAMPs) to activate immune response
• TLR4 recognizes LPS from Gram-negative bacteria
• TLR2 recognizes lipoteichoic acid from Gram-positive bacteria
• NOD2 recognizes muramyl dipeptide from bacterial peptidoglycan
• Activate immune response through signaling pathways and trigger production of pro-inflammatory cytokines and type I interferons

Complement System

• Marks pathogens for destruction, activates immune cells, and inflames tissues
• Classical pathway activated by antibody-bound pathogens
• Alternative pathway activated by pathogens without antibody
• Lectin pathway activated by mannose-binding lectin
• C3 is a central component of the complement system
• C5-9 forms the membrane attack complex
• Opsonization marks pathogens for phagocytosis
• Chemotaxis attracts immune cells to site of infection
• Cytolysis directly kills pathogens

Neutrophil Function

• Phagocytosis: engulfing and digesting pathogens
• Degranulation: releasing enzymes and antimicrobial granules
• Respiratory burst: producing reactive oxygen species (ROS)
• Recognize pathogens through PRRs and Fc receptors
• Activate NADPH oxidase to produce ROS
• Release granules containing enzymes (e.g., elastase, myeloperoxidase)
• First line of defense against bacterial infections
• Rapid response to tissue damage and inflammation

Natural Killer Cell Biology

• Large granular lymphocytes with no antigen-specific receptor
• Spontaneous cytotoxicity against tumor cells and virally infected cells
• Activate through recognition of missing or altered self-MHC molecules
• Activate via activating receptors (e.g., NKp46, NKp30, NKG2D)
• Activate by cytokines (e.g., IL-2, IL-12, IL-15)
• Direct cytotoxicity: killing target cells through granzyme and perforin
• Cytokine production: IFN-γ, TNF-α, and others
• Modulate immune response: regulating T cell and dendritic cell activity