BIOD 331 Module 3/ BIOD 331 Module 3
Study Guide
I. Features of Innate and Adaptive Immunity (Source 3.1)
Immune System Overview
● Immunity = protection from disease (esp. infectious).
● Immune response = coordinated cell activity; may be immediate or delayed.
● Problems arise when excessive, misdirected, or self-reactive.
Innate Immunity (Natural, First Line)
● Immediate, non-specific defense; present before infection.
● Physical/Chemical Barriers → Physical skin, Chemical tears, saliva, mucus, mucus
membranes, stomach acid, urine wash out microbes out of urethra
○ Skin: keratin, acidic/salty environment (inhospitable to microbes), antimicrobial
proteins, lysozymes (enzyme in saliva, tears, mucus)
○ Epithelia: GI goblet cells trap pathogens; respiratory cilia + mucus remove
microbes.
● Internal → Cell Types → come from hematopoietic stem cells in bone marrow, produce
leukocytes and enter the blood stream and go to different tissues for further maturation
and activation.
○ Leukocytes
, ■ Granulocytes → contain granules
● [defensive] Neutrophils – 55% WBCs; early responders; use phagocytosis to kill
microbes.
● Eosinophils – 1–4%; parasitic infections, allergy.
● Basophils – <1%; release histamine, proteolytic enzymes; allergic + parasitic
infections
■ Agrunoloyctes → lack granules
● [largest in size] Monocytes – 3–7%; mature into macrophages/DCs.
Note: Monocytes are the first responder to phagocytose a
foreign invader.
○ [defensive]Macrophages – long-lived, tissue-resident; first
phagocytes encountered. APC
○ Dendritic cells – capture antigens, present to lymphocytes;
bridge innate ↔ initiate adaptive immunity. They serve an
important role between innate and adaptive immunity.
APC
● [defensive] NK cells – kill tumor/infected cells w/o prior exposure(innate); cytokine
production (adaptive)
● Defensive Proteins (antimicrobial proteins) → attack pathogens directly or hinder their
ability to replication
○ interferons (viral infected cells produce these - signal neighboring cells to prepare
for incoming attack allowing them to respond by producing antiviral proteins)
○ Complement system
■ Complement proteins - 30 or so blood proteins, once activate they can
destroy membranes by MAC (membrane attack complex - creates holes in membrane and
cell lysis ● Inflammation
○ Widens blood vessels and increased capillary permeability which lead to redness,
heat, swelling and pain
● Fever → caused by chemicals called pyrogens (caused by bacteria releasing
endotoxins or cytokines released by our immune system → signaling molecules that
tell brain the hypothalamus thermal regulatory center and increases the
temperature set
○ Abnormally high body temp
○ Slows the growth of bacteria; speeds up body defenses
Adaptive Immunity (Acquired, Second Line)
, ● Triggered by antigens (non self/foreign - cancer cells, non-self proteins, bacteria,
viruses, fungi, parasites, pollens, venom, transplants).
● Features: systemic, specific, has memory, self vs. non-self recognition.
● Two types:
1. Humoral – B lymphocytes → antibodies; defense against extracellular
microbes/toxins.
2. Cell-mediated – T lymphocytes; defense against intracellular microbes (e.g.,
viruses).
Antigen Presentation
● APCs (macrophages, DCs) process antigens → epitopes, present via MHC.
● Helper T cells (CD4+) recognize antigen-MHC → release cytokines → activate B cells
(antibodies) + cytotoxic T cells.
● Leads to effector cells (destroy antigens) and memory cells (rapid response on re-
exposure).
Humoral Immunity (B Cells, Antibodies)
● Antibodies (Immunoglobulins – Ig):
○ IgG (75%) – antiviral, antibacterial, antitoxin; crosses placenta.
○ IgA (15%) – mucosal secretions; local immunity; blocks pathogen attachment.
○ IgM (10%) – first produced (fetus, early infection); indicates current infection.
○ IgD – low levels; uncertain function.
○ IgE – allergy, inflammation, parasites.
● Primary response: 1–2 weeks; IgM first, then IgG; memory cells formed.
● Secondary response: faster, stronger (basis for vaccines/boosters).
Cell-Mediated Immunity (T Cells)
Study Guide
I. Features of Innate and Adaptive Immunity (Source 3.1)
Immune System Overview
● Immunity = protection from disease (esp. infectious).
● Immune response = coordinated cell activity; may be immediate or delayed.
● Problems arise when excessive, misdirected, or self-reactive.
Innate Immunity (Natural, First Line)
● Immediate, non-specific defense; present before infection.
● Physical/Chemical Barriers → Physical skin, Chemical tears, saliva, mucus, mucus
membranes, stomach acid, urine wash out microbes out of urethra
○ Skin: keratin, acidic/salty environment (inhospitable to microbes), antimicrobial
proteins, lysozymes (enzyme in saliva, tears, mucus)
○ Epithelia: GI goblet cells trap pathogens; respiratory cilia + mucus remove
microbes.
● Internal → Cell Types → come from hematopoietic stem cells in bone marrow, produce
leukocytes and enter the blood stream and go to different tissues for further maturation
and activation.
○ Leukocytes
, ■ Granulocytes → contain granules
● [defensive] Neutrophils – 55% WBCs; early responders; use phagocytosis to kill
microbes.
● Eosinophils – 1–4%; parasitic infections, allergy.
● Basophils – <1%; release histamine, proteolytic enzymes; allergic + parasitic
infections
■ Agrunoloyctes → lack granules
● [largest in size] Monocytes – 3–7%; mature into macrophages/DCs.
Note: Monocytes are the first responder to phagocytose a
foreign invader.
○ [defensive]Macrophages – long-lived, tissue-resident; first
phagocytes encountered. APC
○ Dendritic cells – capture antigens, present to lymphocytes;
bridge innate ↔ initiate adaptive immunity. They serve an
important role between innate and adaptive immunity.
APC
● [defensive] NK cells – kill tumor/infected cells w/o prior exposure(innate); cytokine
production (adaptive)
● Defensive Proteins (antimicrobial proteins) → attack pathogens directly or hinder their
ability to replication
○ interferons (viral infected cells produce these - signal neighboring cells to prepare
for incoming attack allowing them to respond by producing antiviral proteins)
○ Complement system
■ Complement proteins - 30 or so blood proteins, once activate they can
destroy membranes by MAC (membrane attack complex - creates holes in membrane and
cell lysis ● Inflammation
○ Widens blood vessels and increased capillary permeability which lead to redness,
heat, swelling and pain
● Fever → caused by chemicals called pyrogens (caused by bacteria releasing
endotoxins or cytokines released by our immune system → signaling molecules that
tell brain the hypothalamus thermal regulatory center and increases the
temperature set
○ Abnormally high body temp
○ Slows the growth of bacteria; speeds up body defenses
Adaptive Immunity (Acquired, Second Line)
, ● Triggered by antigens (non self/foreign - cancer cells, non-self proteins, bacteria,
viruses, fungi, parasites, pollens, venom, transplants).
● Features: systemic, specific, has memory, self vs. non-self recognition.
● Two types:
1. Humoral – B lymphocytes → antibodies; defense against extracellular
microbes/toxins.
2. Cell-mediated – T lymphocytes; defense against intracellular microbes (e.g.,
viruses).
Antigen Presentation
● APCs (macrophages, DCs) process antigens → epitopes, present via MHC.
● Helper T cells (CD4+) recognize antigen-MHC → release cytokines → activate B cells
(antibodies) + cytotoxic T cells.
● Leads to effector cells (destroy antigens) and memory cells (rapid response on re-
exposure).
Humoral Immunity (B Cells, Antibodies)
● Antibodies (Immunoglobulins – Ig):
○ IgG (75%) – antiviral, antibacterial, antitoxin; crosses placenta.
○ IgA (15%) – mucosal secretions; local immunity; blocks pathogen attachment.
○ IgM (10%) – first produced (fetus, early infection); indicates current infection.
○ IgD – low levels; uncertain function.
○ IgE – allergy, inflammation, parasites.
● Primary response: 1–2 weeks; IgM first, then IgG; memory cells formed.
● Secondary response: faster, stronger (basis for vaccines/boosters).
Cell-Mediated Immunity (T Cells)
