Quiz 6 Flashcards
Antigen
molecule that triggers the immune response
Innate Immunity
present at birth; always present
not antigen specific
immediate response to infection
1st line of defense
Adaptive Immunity
develops throughout life after initial exposure to antigen
antigen specific
lag time between infection and response
2nd line of defense
Which type of immunity involves memory and may develop lifelong immunity?
Adaptive
-immunological specificity
-immunological memory
Innate immunity cells
neutrophils
monocytes
macrophages
eosinophils
mast cells
NKT-lymphocytes
Adaptive immunity cells
T-lymphocytes
B-lymphocytes
What is the bodies response to infection called?
Host response
Primary function
to defend life of host by identifying foreign substances in body and defending against them by
-developing immune cells that target invaders
-producing biochemical substances to amplify immune response and counteract invaders
Dysfunction Immune/Loss of Immune Response
loss of immune function
can be deadly
ex/ HIV
Overactive Immune Response
can harm body that its trying to protect
ex/ rheumatic heart disease
Neutrophils
1st cells deployed, most abundant
Eosinophils
parasitic infections, collaborate w/ mast cells and basophils to regulate allergic response
Periodontal pathogens are most effectively destroyed by…
PMNs
Basophils
allergic response, coordinates physiological activity
*largest by least common granulocyte
Mast cells
release key inflammatory mediators for allergic response, protect against pathogens
Agranulocytes
no granules, lymphocytes, monocytes/macrophages
PML (polymorphonuclear leukocytes)
multilobulated nucleus, does not include mast cells
Monocytes
single irregular nucleus, no granules, located in bloodstream*
Plasma B cells
make antibodies
Memory B cells
remembers previous exposure and evoke more rapid enhanced response
Fragment Antigen Binding (Fab)
antigen binding region, binds to microbe and helps to kill it
Fragment Constant (Fc)
region at tail end that binds to immune cell and proteins of complement system
*binds to B cell
Major classes of immunoglobulins/antibodies
IgG
IgM
IgA
IgE
IgD
IgG
most abundant, opsonizer (enhances phagocytosis, only one that can pass through placental barrier
IgM
first to respond, largest, pentamer structure (10 binding sites), most efficient in clumping of particles (agglutination)
IgA
principle defense at mucosal barriers, main one in secretions (SALIVA), poor activator of complement system, J chain
IgE
host allergic response, parasites, binds to mast cells and basophils
IgD
least abundant and least understood
T-cells
cell mediated immunity
produces cytokines
T-helper (CD4)
most important, regulates differentiation and maturation of B cells so antibodies are produces, activates cytoxic T cells, induces macrophages
T-cytotoxic (CD8)
neutralizes virally infected cells and tumor cells (direct or indirect)
-impaired function feature of many chronic autoimmune diseases
NKT
naturally kill target, releases massive quantity of inflammatory mediators and other cytokines
NK vs NKT
NK are a separate and distinct category, they mature and develop in circulation, do not require reactivation
Macrophages
largest, highly pagocytic, agranulocyte, located in tissues, important role in chronic perio/inflammation
NK lymphocytes
large granular
larger than B or T cells
both types of immunity attribute
preprogrammed natural killer
*DO NOT REQUIRE PREACTIVATION
4 functions of complement system
- destruction of pathogens
- opsonization of pathogens
- Recruitment of phagocytes
- Immune clearance
Destruction of pathogens
membrane attack complex- protein unit capable of puncturing cell membrane
*known as lysis
Opsonization of pathogens
coats surfaces of bacteria to allow phagocytes to bind and destroy it
Recruitment of phagocytes
additional phagocytes called to infection site
Immune clearance
immunce complexes removed from circulation
“housekeeping”
Attraction of leukocytes to infection site
- migration
- chemotaxis
- Phagocytosis
Transendothelial migration
tissue resident leukocytes release cytokines and chemokines into CT to recruit more leukocytes from bloodstream
*leukocytes squeeze between cells of blood vessel wall to exit bloodstream
extravasation- cell squeezing
Chemotaxis
leukocytes enter CT and drawn to invading pathogens via cytokines and chemokines
swarm like migration pattern of neutrophils- neutrophilic swaming
Phagocytosis process
- bacteria attached to membrane (pseudopodia)
- ingested, forms phagosome
- phagosome fuses w/ lysosome
- lysosomal enzymes digest material
- digested products released from cell
How does phagocytosis result in local tissue destruction?
released enzymes during the process cause damage to local tissues the same way they destroy bacteria tissue
Characteristics of inflammation
dilation of blood vessels
increased permeability of blood capillaries
increased blood flow
leukocyte migration into tissues
Mast cells release…
cytokines, which in turn dilate capillaries and increase vascular permeability (inflammation)
Inflammatory biochemical mediators
biologically active proteins secreted by cells that activate body’s inflammatory response
Chemokines (subgroup of cytokines)
attract immune cells to site of infection or injury and regulates chemotaxis
Inflammatory mediators involved with periodontitis
cytokines, prostaglandins, matrix metalloproteinases (MMP)
Cytokines
name for any protein that is secreted by cells and affects nearby cells, signals immune system to send more phagocytes to infection site
Cytokines involved in periodontits
Interleukin 1 (IL-1)
Interleukin 6 (IL-6)
Interleukin 8 (IL-8)
Tumor necrosis factor alpha (TNF-a)
Prostanglandins
Powerful: D, E, F, G, H, I
PGE: Important role in bone destruction*
-macrophages is major source of PGE
Overproduction of MMPs
breakdown of connective tissue of periodontium
Effects of MMPs
without collagen, degradation of
gingiva -> recession
PDL-> pocket formation
Alveolar bone -> tooth mobility
Acute inflammation
increased movement of plasma and leukocytes from blood to injured tissues
heat, redness, swelling, pain, loss of function
Chronic inflammation
accumulation of macrophages, exaggerated inflammatory response
C-reactive protein
journal of Periodontology 2001
inflammatory effects from oral disease cause oral bacterial byproducts to enter bloodstream. These byproducts trigger liver to make CRP, inflames arteries and promotes blood clot formation
Remission
signs/symptoms disappear partially or completely- chronic inflammation
Exacerbation
sign/symptoms may recur in all of their severity in active period of disease
Goals of inflammatory response
- prevent initial infection/remove damaged tissue
- prevent spread of infection/repair damaged tissue
- recruit effector cells if immune cells of innate system cannot control infection or repair tissues
- mobilize effect cells (T & B lymphocytes)
