Immune Chapter Flashcards
Innate Defenses:
- General, non-specific defenses that all healthy
individuals are born with
Surface Barriers
Skin & mucosal membranes
Internal Defenses
Cells, Antimicrobial proteins, Inflammation, Fever
Innate Defenses: Surface Barriers
Function: Physically and chemically block the entrance of pathogens
External Surface Barrier: Skin
oSpecial Features: Keratinized, stratified squamous epithelium
oExternal Secretions: Sweat, sebum, hyaluronic acid
Internal Surface Barrier: Mucosa
oSpecial Features: Contains MALT
oInternal Secretions: Mucus, saliva, stomach acid (HCl), urine
Innate Defenses: Internal Defenses
- Cells
oPhagocytic, proinflammatory, apoptosis-initiating, parasite-destroying - Antimicrobial Proteins
oIFNs & complement proteins - Inflammation
- Fever
Phagocytic cells
engulf pathogens, foreign
particles, and cellular debris
Proinflammatory cells
release inflammatory chemicals to recruit
immune cells (leukocytosis)
Apoptosis-Initiating cells
secrete perforins to perforate target membranes.
Leads to targets lysing. Secrete granzymes to initiate
target apoptosis (cell suicide).
Parasite-Destroying cells
Secrete enzymes and toxins lethal to parasites
Antimicrobial Proteins: IFNs
Interferons (IFNs) interfere
with protein synthesis to
prevent viral replication.
It protects neighboring cells
from the spread of infection.
Antimicrobial Proteins: Complement
Opsonization
Complement proteins called opsonins bind and tag
targets to attract phagocytic cells
- Enhances Inflammation
Complement proteins activate mast cells and basophils
Complement proteins also attract neutrophils and
macrophages
Antimicrobial Proteins: Complement
- Enhances Cell Lysis (via MACs)
Complement proteins form large membrane channels
called Membrane Attack Complexes (MACs) to cause
cytolysis - Enhances Phagocytosis
Complement proteins link antibody-antigen complexes
to RBCs to be sent to the liver where macrophages will
eliminate the complexes
Inflammation
Immediate, localized response within vascularized
tissues
Signs of Inflammation:
oP = Pain caused by triggered pain receptors
oR = Redness caused by increased blood flow
oI = Immobility (severe swelling can immobilize joints)
oS = Swelling caused by extra-permeable capillaries
oH = Heat caused by increased blood flow
Events of Inflammation
- Injured tissues, macrophages, dendritic cells, basophils, and mast cells secrete inflammatory chemicals (SOS!)
- Blood vessels dilate and become more permeable
- Leukocytosis: Immune cells are recruited to the site of injury
o Margination: WBCs adhere to blood vessel walls
o Diapedesis: WBCs squeeze out of blood vessels
o Chemotaxis: WBCs follow a chemical trail to arrive at the site of injury - Plasma proteins like antibodies, complement proteins, and clotting factors are delivered to the site of injury.
Effects of Inflammation
To promote healing!
o Vasodilation
o Increased capillary permeability
oLymph containing pathogens and dead cells is
drained away
Fever: Pyrexia
Systemic inflammation caused by immune cells secreting pyrogens
Elevated body temperature over 100oF
Benefits of Fever:
Restrict pathogen growth and replication
Promotes IFN activity
Activates macrophages & lymphocytes
Accelerates tissue repair
Risks of High Fevers:
Protein denaturation
Febrile seizures
Brain damage
Death (108 o F)
Cellular Immunity
-Cell to cell combat
-Mediated by T-cells
-Activated by APC’s presenting MHC’s
-Best against intracellular pathogens like viruses and some cancers
Humoral Immunity
-Secrete antibodies to fight pathogens
-Mediated by B-cells
-Activated by exposure to foreign antigens/ exposure to foreign antigens and cytokines from the CD4 cells
-Best against extracellular pathogens in our bloodstream (like bacteria).
Primary Humoral Response
Slow & Weak
Initial exposure = a naïve immune system reacts slowly to the presence of infection and does not secrete a lot of antibodies. You may get sick but if you survive the infection, memory B-cells will do the secondary
response.
