Block A Flashcards
Routes of infection
-person-to-person
-orally
-contaminated water
-living vectors
-fomites (non-living objects)
Innate Immunity definition
- non-specific and inherited
-doesn’t require prior exposure
-protect against foreign cells without recognising specific identity
-recognises general markers on foreign pathogens
Phagocytosis
-engulf and destroy particles by endocytosis
-main phagocytes = neutrophils, monocytes, macrophages, mast cells, dendritic cells
-phagocytes move to area needed by chemotaxis
Lymphoid Organs
-bone marrow
-thymus
-lymph nodes (centered around nose, mouth, lungs, and gut)
-spleen
-peyer’s patch
Lymph Node Areas
Germinal Centre - houses B cells
Paracortical Area - houses T cells
Parafollicular Area - forms interface for B and T communication
Medullary Cords - house plasma cells and macrophages
Spleen Areas
Red pulp - RBCs broken down/produced
White pulp - B, T, and APC interaction occurs
Peyer’s Patch
organised surface receptors in the gut
dendritic cells extend pseudopods into gut to sample antigen
M-CELLS - specialised APC (modified epithelial cells) present directly/indirectly to T cells
Leaving the lymph node
-dendritic cells enter via afferent lymphatics
-T cells enter via HEVs, if antigen recognised leaves via afferent lymphatics. If not, leave via cortical sinuses
Lymphocyte Recirculation following infection
-DCs go to lymph node (via lymphatics)
-Encounter naive T cells
-Activated T cells return to blood
What are PRRs?
Pattern-Recognition Receptors
-innate immune cells detect molecules from pathogens/damaged cells via these
What are PAMPs?
Pathogen-Associated Molecular Patterns
-distinct motifs on pathogens that are recognised by PRRs
What are DAMPs
Damage-Associated Molecular Patterns
-damaged host cells express motifs
Types of PRRs?
Toll-Like Receptors (TLRs) - recognise leucine repeats
C-type Lectin Receptors (CLRs) - recognise carbohydrate repeats
NOD-Like Receptors (NLRs) - recognise peptidoglycans
TLR Structure
Endosomal or Plasma Membrane receptors
Composed of Leu rich pathogen recognition domain AND signaling domain
TLR-Stimulation Consequences
Phagocytic cell activation
1. cytokines & chemokines released
2. increased phagocytosis
3. intracellular killing mechanisms triggered
Types of Cytokines
Chemokines
Interferons
Interleukins (IL)
Lymphokines
Tumour Necrosis Factors (TNF)
Cytokine Roles
IL-1 - inflammation
TNF-alpha - inflammation
IL-12 - induce adaptive immunity
IL-6 - induce adaptive immunity
Interferons - antiviral
Chemokines
Subpopulation of cytokines - cause immune cells to MOVE (eg to site of infection)
Also called Chemoattractants
E.g. IL-8, CCL19, CCL21, RANTES, CCL2 (MCP-1)
Adaptive Immunity Definition
-Specific immunity to each pathogen
-Requires prior exposure
-Takes days-weeks to become established
-Creates immunological memory for long-term protection
Leukocyte Extravasation Steps
- Chemoattraction
- Rolling adhesion
- Tight adhesion
- Endothelial transmigration
Extravasation Key Molecules
Selectins
-endothelial (P-selectin, E-selectin)
-bind carbohydrates on leukocytes
Integrins
-involved with cell adhesion, found on leukocytes
-e.g. LFA-1 binds to CAMs
-e.g. ICAM on endothelial cells
Formation of B cells
-develop in bone marrow, division starts at Haematopoietic Stem Cells
-series of divisions produce common lymphoid progenitors to give rise to B and T cells
-those remaining in Bone Marrow = B cells
-mature B cells move to periphery
Formation of T cells
-develop in bone marrow, division starts at Haematopoietic Stem Cells
-series of divisions produce common lymphoid progenitors to give rise to B and T cells
-those that migrate to the Thymus = T cells
How are B cells matured?
Re-arrangements of gene segments of Ig occur within the cell so that by immature B cell point, unique cell surface IgM (BCR receptor) is formed
