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.
Secondary Response
Rapid & Robust
Subsequent exposures (even years later) will trigger the memory B-cells to react quickly. Their reaction time is so rapid and the secretion of antibodies is so bountiful that we clear infections before we even present with symptoms.
Types of Antibodies
IgM
Fixes and activates complement system. Secreted by plasma cells during primary response
IgA
Prevents pathogens from attaching to epithelia. Found in bodily secretions (like sweat, sebum & saliva)
IgD
Antigen receptors on B cell surfaces
IgG
Fixes and activates complement system. MAIN antibody secreted during primary and secondary response.
IgE
Causes basophils and mast cells to release histamine and other inflammatory chemicals (especially during allergic rx’ns!)
Antibody Action: Binding to antigens will
cause…
Neutralization = Antibodies can surround
targets to block them
Precipitation = antibodies can bind antigens (tiny
proteins)
Agglutination = antibodies can bind
entire cells (like bacteria)
Antibody Action: Exposed stem regions will
promote…
Stem regions of antibodies bind complement proteins to activate them.
Stem regions of antibodies bind to phagocytic cell receptors.
Stem regions of antibodies bind to NK
cells to trigger perforin and granzyme secretion.
Blood Transfusions
Blood typing ensures that no agglutination happens.
Agglutination occurs when antibodies recognize foreign
RBC antigens.
Tissue Grafts/ Organ Transplantation
Tissue typing along with immunosuppressive therapy
ensures that donated tissues and organs are not
rejected by recipients.
SCIDs
Severe Combined Immunodeficiencies, primary congenital immunodeficiency where an infant is born missing components of the immune system. AKA “Bubble Boy Disease”
Hypersensitivity
Allergies. Abnormal and exaggerated immune responses
