30.3 - Defence Against Infectious Disease_Innate Mechanisms Flashcards
What is the difference between the innate and the specific immune response?
The immune system is divided into nonspecific (innate) and specific (adaptive) responses. Nonspecific defences, like skin and stomach acid, block pathogens indiscriminately. Specific defences, such as B and T lymphocytes, adapt to specific pathogens after exposure.
Give examples of how the innate and specific immune responses interact.
*Dendritic cells activate T-cells -> major mode of communication between the 2 responses.
*Abs bind to phagocytes Fc region to increase efficiency of recognition.
*CKs secreted by T cells improve effectiveness of innate immunity.
List the cells of the innate immune system
Leukocytes:
-Neutrophils
-Eosinophils
-Basophils
-Monocytes
-Mast cells
-Macrophages (tissues)
-Dendritic cells
What are the barriers to infection?
Skin, mucus, gastric acid, bile salts, normal microbiota.
How do innate immune cells detect pathogens?
Innate immune cells have pattern recognition receptors (PRRs) that recognise a molecular pattern called a pathogen associated molecular pattern (PAMP) on the surface of microbes
Name the four PRRs
Toll like receptors (TLRs)
C type lectin receptors
NOD-like receptors (NLRs)
RIG-I Helicase receptors (nucelic acid receptors)
What are inflammasomes?
They are innate immune system receptors/sensors that regulate the activation of caspase-1 + induce inflammation in response to infectious microbes and molecules derived from host proteins.
What are the different effector functions in the innate immune response??
- Respiratory burst
- Degranulation
- Phagocytosis + phagolysosomal degradation.
What is respiratory burst?
the rapid release of the reactive oxygen species (ROS), superoxide anion (O 2) and hydrogen peroxide (H 2O 2), from different cell types.
Which cells perform respiratory burst?
Neutrophils, monocytes, and macrophages.
Which cells degranulate?
Mast cells, eosinophils, basophils.
Which cells are capable of phagocytosis and phagolysosomal degradation?
Neutrophils and macrophages.
How does opsonisation aid phagocytosis?
Opsonins, such as antibodies (IgG, IgA) and complement proteins (C3b, C4b), bind to the surface of pathogens. This binding facilitates the attachment of pathogens to phagocytes (macrophages and neutrophils) through Fc receptors on the phagocytes.
What are natural killer cells?
Cytotoxic lymphoycte which kill virus infected cells and tumour cells
They produce IFN- gamma which activates macrophages to kill ingested bacteria
What soluble molecules are involved in the innate immune response?
Complement, (Classical, alternative and MBP pathways), type 1 interferons (alpha and beta), type 2 interferon (gamma) and other secreted molecules.
Give an example of an innate immune evasion strategy.
Avoidance of phagocytosis by capsules (e.g. Streptococcus)
*leukocyte attachments and ROS-induced breakdown become more challenging
What are the chemical barriers to infection? How do they work?
*Gastric acid (HCl) - denatures proteins and kills pathogens
*Bile salts - inhibit binary fission and regulate gut inflammatory pathways
*Surfactant - binds to surface of microbes to facilitate phagocytosis
*Antimicrobial peptides - (Defensin) made throughout skin and mucous *Membranes - highly positively charged that create pores in lipid membranes of pathogens
What are the mechanical barriers to infection?
*Skins epidermis - keratinised squamous epithelial cells
*Mucous membranes - Coated in mucins (sticky mixture making penetration of respiratory, GI and genitourinary infections more difficult)
What is the mechanism of action of type I interferons?
ANTIVIRAL = BLOCK SYNTHESIS OF VIRAL PROTEINS
They have NO effect on extracellular virus particles
Bind to cell surface
Signals to the cell to synthesise three antivral proteins
What is the mechanism of action of type II interferons?
Active against intestinal viruses (rotavirus and norovirus)
