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72 Cards in this Set

  • Front
  • Back
What is immunity?
All mechanisms by which the body protects against foreign agents
Two “arms” of immune response
Innate immunity(non-specific)
-born with
-fast acting
-barriers, cells, and serum proteins

Acquired (adaptive) immunity(specific)
-improves with exposure
-primarily mediated by lymphocytes (T and B cells)
Examples of Innate defenses
-Barriers (e.g. skin, mucous membranes)
-Chemical mediators
-Interferon (fight viral
-Complement (C.L.I.O)
-Toll-like receptors
-NK cells (recognize tumor or viral cells – “altered-self cells”
Two major surfaces by which most microbes/Ag enter body:
-Mucous membranes
Live and Dead cells with keratin
Epidermis is renewed every _____ days
When Epidermis is damaged it secretes _______ and _____
IL-8 / Tumor Necrosis Factor(TNF) (inflammatory)
Dermis is ________ and contains (3) _________
Hair follicles,
Sweat glands, &
Sebaceous glands (oil can coat microbes)
Langerhans cells (DC) in skin
move Ags to LN
Normal flora in skin
Can inhibit pathogenic microbes
Restriction enzymes
enzymes in skin that restrict growth of viruses
inhibit bacteria in skin (ex. colicins)
Innate defenses of skin


Langerhans cells (DC)

Normal flora
Mucous membranes
Respiratory, Digestive, Genitourinary Tracts
sIgA (secretory immunoglobulin) is an ________ componant of mucus membrane immune function
coats (traps) microbes
Mucociliary escalator
– movement of mucous up to be expelled (cough/sneeze) or swallowed
examples of 2 pathologies associated with mucociliary escalator
Cystic fibrosis patients – abnormal cilia and mucous

Smoking – temporary paralysis of cilia
Lysozyme functions by
cleavage of bacterial cell wall (b1,4 linkage of peptidoglycan)
immune defences in mucus membranes
secretory immunoglobulin [sIgA](adaptive)
& Mucin and Lysozyme
Respiratory tract contains ________ which is important in immune function
-Pathogen-binding proteins
-Important in alveolar function
Surfactants are members of ________ family
Surfactants bind _______ and ________
pathogen and phagocytes
Surfactants binds pathogen and phagocytes using
Globular lectin-like “head” to bind _____ and a Collagen-like “tail” to interact with ______
an example of surfactant is __________ which can activate complement proteins
Mannan-binding lectin (MBL)
Chemical mediators of innate defenses
Stomach acid/digestive enzymes
Complement cascade
Lysozymes are involved in
destruction of microbes
Interferon has _______ activity
Complement cascade has _______ activity and consists of (3)
antimicrobial/Cell lysis, opsonization, inflammation
the low _____ of stomach acid helps to kill microbes
Reduced acid production increase risk for ______ infections
Some microbes can overcome the low pH of the stomach. For example, ___________ creates microenvironments where pH is not as low
Helicobacter pylori
Interferon has _________ properties
Interferon causes cells to become resistant to viral infection by inducing changes in _________ and inhibiting _________
cell surface receptors/viral replication
Interferon inhibits viral replication by (2) ________
inducing CHANGES in host cell molecules needed for viral replication and
stimulating of APOPTOSIS of infected cells
types of interferon
alpha, beta, and gamma
a and b IFN have ________ than g IFN
more potent antiviral properties
a and b IFN are involved in activation of ______ activity and
increased activity (class I presentation)
NK cell /TAP
g IFN is involved in
immune system activation
g IFN is produced by
Th1 cells
series of enzymes that chop up proteins for presentation w/ class I, role inCD8+ cells
What are the three activities of alpha and beta IFN
1) induce resistance to viral replication in all cells by destroying viral mRNA
2)Increase MCH class I expression and Ag presentation in all cells by increased recognition of CTL or cytotoxic T lymphocytes.
3)Activate NK cells to kill virus-infected cells
cytotoxic T lymphocytes.
phagocytosis involves ________ by _________
Recognition, ingestion, and digestion/Monocyte/macrophage, neutrophil
Resident (tissue) macrophages (Mf)
First cells to encounter microbe
Resident (tissue) macrophages (Mf) are activated by
-molecules on microbes binding to toll-like receptors (TLRs)
-Antibodies (Abs) coating microbe
e.g., of Resident (tissue) macrophages (Mf)
alveolar Mf (lung), Kupffer cells (liver), osteoclasts (bone), microglial cells (brain), histiocytes (CT), mesangial cells (kidney)
Neutrophils vs. Monocytes/Mf?
Rapid increase during the acute phase response
Found in healthy tissues
Macrophage or Neutrophil?
Short lived (die after phagocytosis)
Macrophage or Neutrophil?
Rapidly form pus
Macrophage or Neutrophil?
Long lived (survive phagocytosis)
Macrophage or Neutrophil?
Only found in inflamed tissues
Macrophage or Neutrophil?
Slowly form granuoloma (with T cell help
Macrophage or Neutrophil?
Slight increase in blood during inflammation
Macrophage or Neutrophil?
How do macrophage/neutrophils recognize of microbes
1) Changes in adhesion molecules
Extravasation (neutrophils go through the endothelial cells to get to microbe)

2) Acute phase proteins-
Opsonize microbe

3) Microbe specific receptors
CR4 and CD14 – neutrophil binding to LPS
Toll-like receptors
Mf recognition of microbes
Most receptors on Mf bind microbe molecules NOT
found on human cells
Toll-like receptors
-transmembrane signalling protein on Mf or neut used in innate defenses for recognition of microbes
-Many different forms (~10)
-Can bind to many substances (LPS, DNA, RNA, yeast cell wall components)
Upon stimulation of TLRs
get inflammatory response
Neutrophil localization to site of infection
Neutrophil “rolling”
(a/k/a IL-8)
small molecule involved in inflammation
Neutrophil recognition of microbes
CR = complement receptors
FcR = binds to Fc region of Ab
Cytokines (e.g., IL-1B; TNF-a) are
regulatory produce a variety of responses including fever, inflammation etc.
Acute phase response
some cytokines produced by macrophages (IL-6, TNF-alpha, IL-1) float away from site of inflammation/damage to the liver and cause hepatocytes to produce C-reactive protein (CRP) and MBL (mannan-binding lectin). These molecules bind to sugars on microbe to allow for opsonization & complement activation
Septic shock
Occurs when TLR and other receptors on Mf & neuts recognize microbe and over produce inflammatory cytokines (e.g., TNF-alpha) resulting in a systemic inflammatory reaction.
Destruction of ingested microbe results in
Respiratory burst (increased oxygen consumption) within phagocytic cell and production of reactive oxygen and nitrogen intermediates designed to kill the microbe
Purpose of inflammation-
vasodialation draw more WBCs to area
chronic inflammation
NK cells
-Considered to be a lymphocyte but NOT antigen specific.
-Kill virally-infected cells and tumor cells (altered self cells-changes in surface proteins)
-once bind to cell they release lytic mediators
How does NK cell know to kill altered self cell
altered self cell will be lacking some sort of surface marker
Temporal relationship between innate and adaptive immunity
Temporal relationship between innate and adaptive immunity
Some damage occurs in the body for example the epithelial cells. (t=0) Phagocytic cells (neutrophils, monocytes) get called to the area. They release cytokines.(t=2hr) Cytokines stimulate inflammation.(t=4hr) Cytokines can activate compliment (cell lysis, inflammation, opsinization). Cytokines call in NK cells. (t=12hr ) The story may stop here. If microbe not destroyed, then B or T cells called to the area (t=1D). The B cells then produce effector antibodies and the T cells produce effector cytokines.