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Chapter 21: Immune System

Pathogens —agents capable of producing disease

Include viruses, bacteria, fungi, protozoa, helminthes

Fig14.

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HOST

DEFENCES

Innate and Acquired Host Defenses

The second line of defense is a

cellular and chemical system that

comes immediately into play if

infectious agents make it past the

surface defenses. Examples include

phagocytes that destroy foreign

matter, and inflammation which holds

infections in check.

The third line of defense includes

specific host defenses that must be

developed uniquely for each microbe

through the action of specialized white

blood cells. This form of immunity is

marked by its activity toward specific

pathogen s and development of

memory.

Innate,

nonspecific

Acquired,

specific

B and T lymphocytes,

antibodies, cytotoxicity

Second line

of defense

First line

pf defence

Physical

barriers

Chemical

barriers

Genetic

barriers

Inflammatory

response

Interferons Phagocytosis Complement

The first line of defense is a

surface protection composed of

anatomical and physiological

barriers that keep microbes

from penetrating sterile body

compartments.

Third line

of defense

Fig14.

Sebaceous

glands (fatty

acids)

Tears

(lysozyme)

Mucus

Saliva

(lysozyme,

lactoferrin,

peroxidase)

Commensals

Intact

skin

Wax

Low pH

Cilia

Sweat

Defecation

Urination

Paneth

cells

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Stomach

acid

Mucus

Intestinal enzymes

Mucus

physical barriers and their

chemicals

Skin

Mucous membranes

Guard Hairs

Cilia

Mucus

Sweat

Urine

Saliva

“good” bacteria

First Line of Defense: Non specific

NON SPECIFIC DEFENSES: EXTERNAL BARRIERS

1. Skin: Tough (keratin), dry and nutrient-

poor for microbial growth

Acid mantle: thin film of lactic and fatty

acids from sweat and sebum that inhibits

bacterial growth

• Antimicrobial peptides in the skin that kill

microbes

2. Mucous membranes

Digestive, respiratory, urinary, and

reproductive tracts are open to the exterior

and protected by mucous membranes

• Mucus physically traps microbes
• Lysozyme: enzyme destroys bacterial cell

walls

3. Subepithelial areolar tissue

Viscous barrier of hyaluronic acid

Hyaluronidase—enzyme used by pathogens

to make hyaluronic acid less viscous

Second Line of Defense: Inflammatory Reaction

General purposes of inflammation

Limits spread of pathogens, then

destroys them

Removes debris from damaged

tissue

Initiates tissue repair

Four cardinal signs of inflammation

Redness, swelling, heat, pain

Basis for the four cardinal signs of

inflammation

Heat: results from hyperemia;

increases metabolic rate, speeds

mitosis, and tissue repair

Redness: due to hyperemia, and

extravasated RBCs in the tissue

Swelling (edema): due to increased

fluid filtration from the capillaries

Pain: from direct injury to the nerves,

pressure on the nerves from edema,

stimulation of pain receptors by

prostaglandins, bacterial toxins, and

bradykinin; makes us limit of injured

part

Edema contributes to tissue cleanup

Reduces venous drainage ; promotes lymphatic

drainage

Lymphatics collect and remove bacteria, dead cells,

proteins, and tissue debris better than blood capillaries

Platelet-derived growth factor is secreted by blood platelets

and endothelial cells in injured area; Stimulates tissue repair

Hyperemia delivers oxygen , amino acids, and other

necessities for protein synthesis

Fig14.

Degrades virus

nucleic acid

Blocks virus

replication

Virus

release

Assembly

of viruses

Viral

nucleic acid

Virus

infection

Infected

cell

Nearby

cell

Attachment of IFN

to special receptor

Synthesis of antiviral proteins

Signals

activation of genes

Synthesis

of IFN

IFN

gene

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Second Line of Defense: Protective Proteins

Secreted by virally infected cells to “warn” the uninfected

Also activates macrophages and NK cells

a) Interferon

Opsonin: any

substance that

binds pathogens

and make them

more susceptible to

phagocytosis

Antibody and

complement protein

C3b increase

phagocytic action of

immune cells in the

process of

opsonization

THE ACTION OF A NATURAL KILLER CELL

Constant surveillance for pathogens and diseased host cells

Attack and destroy bacteria, transplanted cells, cells infected with viruses,

and cancer cells

Release proteins called perforins punch holes in “sick” cells

Secrete granzymes degrade cellular enzymes and induce apoptosis

(programmed cell death)

THE COURSE OF A FEVER

Figure 21.

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Temperature (°C)

37

39

38

2

4

3

1

5

6

Infection ends,

set point returns

to normal

Defervescence

(body temperature

returns to normal)

Stadium

(body temperature

oscillates around

new set point)

Onset

(body temperature rises)

Normal body

temperature

Hypothalamic

thermostat is

reset to higher

set point

Infection and

pyrogen secretion

Stages of fever: Onset, Stadium, Defervescence

THIRD LINE OF DEFENSE: ADAPTIVE IMMUNITY

Two characteristics distinguish immunity from nonspecific

resistance

1. Specificity: immunity directed against a particular pathogen

2. Memory: when re-exposed to the same pathogen, the body

reacts so quickly that there is no noticeable illness

Lymphocytes: Three basic categories: T, B, and NK cells

Circulating blood contains

80% T cells

15% B cells

5% NK cells (not specific)

Adaptive immunity occur in three stages (RRR)

1. Recognition

2. Attack (React)

3. Memory (Remember)

Natural active immunity Production of

one’s own antibodies or T cells as a result

of infection or natural exposure to antigen

Artificial active immunity Production of

one’s own antibodies or T cells as a result

of vaccination against disease

Vaccine: dead or attenuated (weakened)

pathogens; stimulates the immune

response without causing the disease

Booster shots: periodic immunizations to

stimulate immune memory to maintain a

high level of protection

Types of Acquired Immunity

ANTIGENS

Antigen—any molecule that triggers an immune response

Proteins, polysaccharides, glycoproteins, glycolipids

Characteristics enable body to distinguish “self” molecules

from foreign ones

Epitopes (antigenic determinants)—certain regions of an antigen

molecule that stimulate immune responses

Haptens—too small to be antigenic in themselves

Can trigger an immune response by combining with a host

macromolecule and creating a complex that the body

recognizes as foreign

Cosmetics, detergents, industrial chemicals, poison ivy, and

animal dander

CELL MEDIATED RESPONSE: ANTIGEN-PRESENTING CELLS

T cells cannot recognize antigens on their

own. Antigen-presenting cells (APCs) are

required

Dendritic cells, macrophages, reticular

cells, and B cells function as APCs

MHC: Act as cell “identification tags”

that label every cell of your body as

belonging to you

Structurally unique for each individual,

except for identical twins

Antigen processing

APC encounters antigen

Internalizes it by endocytosis

Digests it into molecular fragments

Antigen presentation

Displays relevant fragments (epitopes)

in the grooves of the MHC protein

Migrates to nearest lymph node

Displays it to the T cells

When T cells encounter a displayed

specific antigen on the MHC protein,

they initiate the immune response

ANTIGEN-PRESENTING CELLS

Figure 21.21a 21- 20

Phagosome

Epitopes

MHC protein

(a)

2

3

4

5

6

1 Phagocytosis

of antigen

Lysosome

Lysosome

fuses with

phagosome

Antigen and

enzyme mix in

phagolysosome

Antigen is

degraded

Antigen

residue is

voided by

exocytosis

Processed

antigen

fragments

(epitopes)

displayed on

macrophage

surface

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