The immune system

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 Simplified Overview of Innate and Adaptive Defenses

Surface barriers (1st line)

Innate • Skin
Defenses • Mucous membranes
• No memory
• Acts within minutes
• Non-specific
Internal defenses (2nd line)
• Phagocytes
• Natural killer cells
• Inflammation
• Fever

Adaptive Humoral immunity

Defenses (3rd line • B cells
of defense)
• Memory
• Takes longer
• specific
Cellular immunity
• T cells
 Simplified Overview of Innate and Adaptive Defenses
Surface barriers (1st line)
• Skin: sweat/sebum = anti-bacterial properties
• Mucous membranes: Trap virus
• Cilia: moves virus towards pharynx to be swallowed = gastric juices very acidic, destroys
pathogen
• Vagina: acidic, inhibits growth of bacteria and fungi
• Tears and saliva: contains lysozyme (enzyme) that destroys pathogens

Let’s look at how the body defends against its first exposure to
influenza virus.

First Line of Defense: Surface Barriers

The mucous membrane lining the airways helps prevent the virus
from entering the body.
Cilia sweep contaminated mucus toward
the pharynx, where it is swallowed and Cilia
Mucus
digested. Virus
Bronchiole
Second Line of Defense: Innate Internal Defenses
Bronchiole

Inflammatory
chemicals 2. Phagocytes (e.g., resident macrophages) engulf
viruses and “sound the alarm” by releasing
inflammatory chemicals.
3. Inflammation brings more immune cells and
plasma proteins to the area by dilating
Capillary arterioles and increasing capillary permeability.
permeability
1.
Arteriole
dilates

1. NK cells recognize virus-infected cells

through the Human Leukocyte antgen (HLA)
Perforins • Secretes perforins: apoptosis

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Internal defenses (2nd line) to physical trauma
• Inflammation : four distinguishing features of short term (acute) inflammation: Heat, Redness, Pain, Swelling

Tissue injury/
pathogens

Release of inflammatory chemicals:

Histamine, kinins, prostaglandins, complement

Inflammatory Attract neutrophils,

2. Increased capillary
chemicals 1. Arterioles dilate permeability monocytes, and
diffusing from
the inflamed lymphocytes to
site act as Local hyperemia area (chemotaxis)
Capillaries leak fluid
chemotactic (increased blood (exudate formation)
agents. flow to area)

Leaked protein-rich
fluid in tissue spaces Leaked clotting Phagocytosis of
proteins form clots pathogens, area
Heat Redness Pain Swelling cleared of debris

Locally increased Possible temporary Fibrin patch forms

temperature increases impairment of Scaffolding for repair
metabolic rate of cells function

Healing
 Simplified Overview of Innate and Adaptive Defenses

Surface barriers (1st line)

Innate • Skin
Defenses • Mucous membranes
• No
memory
• Acts within Internal defenses (2nd line)
minutes • Phagocytes
• Non- • Natural killer cells
specific • Inflammation
• Fever

Adaptive Humoral immunity

Defenses (3rd line • B cells
of defense)
• Memory
• Takes longer
• specific
Cellular immunity
• T cells
 Adaptive defenses: 1. Humoral immunity = production of antibodies
a. Primary response (initial encounter with antigen)

Antigen
Antibody binds B cell and activates it.
This causes
• Multiplication of B cells to
form lots of clones (called
Activated B cells memory cells)
• Differentiation of B cells into
plasma cells that make lots of
Proliferation antibody to the antigen. This
to form a Differentiation of B cells takes 3-6 days. Antibodies
clone
produced 4-7 days later

Secreted
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b. Secondary response : (can be years later)

Memory cell binds antigen and makes plasma cells within hours.
Antibodies are made within 1-2 days

Clone of cells Subsequent

identical to challenge by same
ancestral cells antigen results in
more rapid response

Plasma
cells

Secreted
antibody Memory
molecules B cells

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 Secondary immune response to
Primary immune antigen A is faster and larger; primary
response to antigen immune response to antigen B is
Primary immune response: cell proliferation A occurs after a delay. similar to that for antigen A.
and differentiation upon exposure to antigen
for the first time
• Lag period: 3 to 6 days

Antibody titer (antibody concentration)

• Peak levels of plasma antibody are
104
reached in 10 days

in plasma (arbitrary units)

• Antibody levels then decline
103

Secondary immune response: Re-exposure to

same antigen gives faster, more prolonged, more 102
effective response
• Sensitized memory cells provide
immunological memory 101 Anti-
Anti-
• Respond within hours, not days bodies bodies
• Antibody levels peak in 2 to 3 days at much to A to B
100
higher levels 0 7 14 21 28 35 42 49 56
• Antibodies bind with greater affinity
• Antibody level can remain high for weeks to First exposure Second exposure to antigen A;
months to antigen A first exposure to antigen B

Time (days)
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 Humoral
immunity

Active Passive

Naturally Artificially Naturally Artificially

acquired acquired acquired acquired
Infection; Vaccine; Antibodies Injection of
contact with dead or passed from exogenous
pathogen attenuated mother to antibodies
pathogens fetus via (gamma
placenta; or globulin)
to infant in
her milk
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 Antibodies
• Antibodies—also called Immunoglobulins (Igs)—are proteins
secreted by plasma cells
• Make up gamma globulin portion of blood

• Grouped into one of five Ig classes: IgM, IgA, IgD, IgG, and IgE
How do antibodies get rid of pathogens?

1. Neutralization Neutralization
Simplest, but one of most important defensive mechanism
Antibodies block specific sites on viruses or bacterial exotoxins
Prevent antigens from binding to receptors on tissue cells
Antigen-antibody complexes undergo phagocytosis

2. Agglutination (cells) and Precipitation (soluble molecules)

Soluble molecules or cells are cross-linked into complexes
Complexes are easier for phagocytes to engulf
Agglutination Precipitation phagocytosis
 Table 21.5-1 Immunoglobulin Classes

IgM is first antibody made during primary response, but

plasma cell then switches to IgG for secondary response

• Almost all secondary responses are IgG

• Diagnostically useful: IgM in plasma = current infection but
IgG in plasma indicates older infection (or vaccination)

IgA is found in saliva, sweat, breastmilk, stops

pathogens from attaching to cells (like on mucous
membranes, epidermis)

Table 21.5-1 Immunoglobulin Classes


IgD is another type of antibody
IgG is
• most abundant in plasma
• Protects against bacteria, viruses,
toxins
• Crosses the placenta and gives
passive immunity to fetus
IgE
• Cause basophils to realease
inflammatory chemicals
• Causes mast cells to release
histamine and Triggers allergic
reactions
Mast cell antibodies
IgE
Granules containing
histamine
Mast cell granules
release histame
after allergen/antigen
binds with IgE antibodi
Histamine causes:
• blood vessels to dilate become leaky,
promotes edema;
• stimulates secretion of large amounts
of mucus;
• causes smooth muscles to contract
• If this occurs in in resp system:
Constriction of small respiratory
passages (bronchioles) = asthma
Adaptive defenses: 2. Cell mediated immunity: T cells kill infected cells

Lymph node
1. Antigen presenting cells (APCs) like
1. macrophages, dendritic cells engulf viruses and
dead virus-infected cells.
2.
2. APCs migrate to a lymph node where they
activate T lymphocytes.
APC
3. 3. APCs activate T cells, which forms a clone of
cytotoxic T (TC) cells and memory cells.

4. TC cells divide, enter blood and migrate to site

Tc cells of infection. They attack and kill the infected
Memory Tc cell
cells (like NK cells) .

4.
Perforins
 Autoimmune Diseases: Self study
• Autoimmune disease results when immune system loses ability to
distinguish self from foreign

• Autoimmunity: production of autoantibodies and sensitized TC cells

that destroys body tissues
 Autoimmune Diseases
• Examples
• Rheumatoid arthritis: destroys joints

• Multiple sclerosis: destroys white matter myelin

• Graves’ disease: destroys thyroid causes hyperthyroidism

• Type 1 diabetes mellitus: destroys pancreatic cells

• Systemic lupus erythematosus (SLE): affects multiple organs

 Autoimmune diseases
• Treatment of autoimmune diseases

• Suppress entire immune system

• Anti-inflammatory drugs, such as corticosteroids

• Blocking molecules that activate effector cells (B and T cells)