Sweep 1.1 Flashcards
Mediators of innate immunity:
Prostaglandins
Matrix metalloproteinases
Proteinase inhibitors
Antimicrobial peptides
Prostaglandins (especially PGE2) induce
vasodilation and cytokine production
PGE2 induces
production of matrix metalloproteinases by fibroblasts and osteoclasts, which damage periodontal tissues
Mediators of innate immunity: Matrix metalloproteinases
Degrade extracellular matrix
Example: PMN collagenase (degrades the major structural protein in gingiva)
Concentrations are higher in inflamed gingiva than in healthy gingiva
Mediators of innate immunity: Proteinase inhibitors
Antagonize inflammation
Inhibit degradation of matrix proteins
Alpha-2 macroglobulin: broad spectrum proteinase inhibitor
Alpha-1 antitrypsin: broad spectrum proteinase inhibitor and potent inhibitor of PMN collagenase
Mediators of innate immunity: Antimicrobial peptides
Defensins:
Calprotectin:
Defensins: Inhibit
bacteria and fungi. Produced by mucosal surfaces and salivary gland epithelium.
Calprotectin:
Inhibits bacteria and fungi by chelating zinc. Produced by epithelium, PMNS, monocytes, macrophages.
Acute inflammation or injury increases vascular permeability, resulting in redness, edema, and increased
gingival crevicular fluid flow
PMN deliver
antimicrobial substances to bacteria in the early stages of infection
T-cell receptor has
T-cell receptor has 2 glycoprotein chains ( and ) with variable segments
Variable segments determine the
type of immune response
TCR in periodontitis
different before and after therapy
TCR different between
chronic and aggressive periodontitis
2 types of T-helper cells -
differ in cytokine profiles
Cytokines are messenger proteins that
transmit signals to other cells
Th1: IL-2, IFN-gamma, TNF-alpha
Th2: IL-4, 5, 6, 10, 13
3Cytotoxic T cells (Tc) activated by
cytokines
Tc cells respond to
intracellular pathogens
Antigens from these pathogens bind
MHC I molecules
Tc cells recognize this antigen presentation and
destroy infected cells
Not many Tc cells are found in
periodontitis, suggesting that viruses and invasive bacteria are not major players
B cell response
Humoral immunity
(antibody mediated) triggered in response to soluble antigens
Ag-Ab complex activates
complement
Ag-Ab complex facilitates
opsonization
Th-2 cytokines activate
B cells to plasma cells
2 types of B cells-
Conventional:
produce antibodies against bacteria, levels decrease in healthy and treated sites
Autoreactive:
produce auto-antibodies, levels do not decrease after treatment