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Immune System
Chp. 9
Prokaryotic cells vs Eukaryotic
cells
• All Bacteria
• Organelles present
• No membrane bound
organelles
• DNA stored as chromosomes
• single circular DNA molecule
• No true sexual reproduction adapt fast
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• Sexual reproduction (different
types)
• Eg. Human cells
Eukaryotic Cells, Bacteria, and
Viruses
e.g. human cells
Inject their DNA into
host cells in order to
reproduce Figure 9.2
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Pathogens: Bacteria
• Characteristics:
• Prokaryotic
• Single celled
• Use of variety of resources for growth &
reproduction
• Reproduce & adapt quickly!!
• Types of Bacterial Infections:
• E.g. Pneumonia, tonsillitis, tuberculosis,
botulism, toxic shock syndrome, syphilis,
Lyme disease.
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Determination of Health Risk
• Transmissibility: how easily is it passed from
person to person
• Mode of transmission: respiratory, fecal-oral,
body fluids
• Virulence: how much damage caused by infection
& how rapid is the onset
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Lymphatic System:
RECALL that lymph is defined as fluid derived from interstitial
fluid transported by lymphatic vessels.
Functions:
• Maintenance of blood volume in cardiovascular
system
• Transport fats & fat soluble material from
digestive system
• Filtration of foreign material to defend against
infection
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Lymphatic System: Components
• Lymph: protein-containing fluid transported by
lymphatic vessels
• Lymph nodes: cleanses lymph by filtering out
materials
• Spleen: cleanses blood, removes dying red blood
cells, helps fight infection
• Thymus: secretes chemicals to cause T
lymphocytes to mature
• Tonsils: protects throat
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Physical and Chemical Barriers
Include:
Skin
Tears
Saliva
Earwax
Digestive acids
Mucous
Vomiting
Urination
Defecation
Resident bacteria
Table 9.1
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First Line of Defense: Skin
Physical & chemical barriers:
1. Skin: characteristics of barrier
• Structure: dead layer, inhospitable to
microorganisms
• Constant replacement: many adhering
microorganisms removed
• pH = 5-6. pH too acidic for many microorganisms
to survive in or penetrate.
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First Line of Defense cont.
tears, saliva, earwax, digestive acids, mucus,
vomiting, urination, defecation, resident
bacteria (normal flora)
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Nonspecific Defenses: Second Line
Phagocytes - neutrophils & macrophages
digest “foreign” cells
Natural killer cells - chemically dissolve tumor cells &
virus-infected cells
Inflamatory response - attracts phagocytes & promotes
healing by increasing circulation to area
Interferons - stimulates producing proteins that
interefere w/ viral reproduction
Fever -
helps to fight infections
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The Inflammatory Response
Figure 9.7
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Nonspecific Defenses: Second Line
Inflammatory response
• Signs: redness, warmth, swelling, pain
• Process:
1. tissue damage causes release of histamine
2. blood vessels dilate
3. proteins mark bacteria
4. phagocytic cells arrive & remove invading
microorganisms
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Cells and Proteins Involved in
Specific Defenses
Table 9.3
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Specific Defense Mechanism: Third
Line
Immune response:
• Antigens: major histocompatibility complex
(MHC) proteins that are part of the cell
membrane or cell wall of viruses & bacteria.
Once identified as an “invader” they trigger
immune response.
• B cells: produce circulating antibodies against
an antigen.
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Antibody Structure & Function:
The antigen binding site is
specific to the protein coat of
a given bacteria or virus
(species specific).
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Attachment of an antibody
Now marks the “invader” for
ingestion by phagocytotic cells
(eg. WBC)
Figure 9.11
Line of Defense: Third Line
T cells: type of lymphocytes, recognize pathogen
antigens, then attach to and kill pathogen.
• Helper T cells: stimulate other immune cells
• Cytotoxic T cells: kill abnormal & foreign cells
• Memory T cells: reactivate on re-exposure
• Suppressor T cells: suppresses other immune
cells
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The Basis of Immunity
Following 1st exposure ,
antibody response
declines after
approximately
1 month.
Re-exposure to
the same antigen
Results in a more
Rapid, stronger,
longer lasting
immune response.
Figure 9.15
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Immune Memory Creates Immunity:
Primary Immune Response
• Process: recognition of antigen, production and
proliferation of B and T cells
• Characteristics: lag time of 3-6 days for
antibody production, peak at 10-12 days
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Immune Memory Creates Immunity:
Secondary Immune Response
• Process: recognition of antigen, production and
proliferation of T cells and plasma cells
• Characteristics: lag time in hours, peak in days
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Medical assistance in the War
Against Pathogens
• Active immunization: effective against viruses
• Passive immunization: effective against existing
infections
• Monoclonal antibodies: clones of hybrid cells
• Antibiotics: effective only against bacteria,
resistance is a problem. They act by disrupting
the mitotic reproduction of bacteria. Not
effective against viruses due to means by which
viruses reproduce [see earlier ppt]
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Tissue Rejection
• Transplants: 75% match essential
• Recent advances: improvements in
immunosuppressive drugs, better techniques for
tissue typing, national organ bank systems
• Immunosuppressive drugs: prevent patient’s
immune system from attacking transplanted
tissue
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Inappropriate Immune Responses
• Allergies: hypersensitivity reaction, excessive
inflammatory response mediated by IgE
• Localized: affect only the area exposed
• Systemic: affect several organ systems
• Anaphylactic shock: severe systemic allergic
reaction
• Symptoms: difficulty breathing, severe
stomach cramps, swelling throughout the
body, circulatory collapse, fall in blood
pressure
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Inappropriate Immune Responses:
Autoimmune Disorders
• Defective recognition of “self”
• Lupus Erythymatosis (LE or Lupus):
inflamed connective tissue
• Rheumatoid Arthritis:
inflamed synovial membrane
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The Structure of HIV
Figure 9.19
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Immune Deficiency: AIDS
• HIV targets cells of your immune systemdisabling it
• HIV Retrovirus attaches to the immune system’s
T helper cells [recall these cells stimulate
production of other immune cells].
• HIV Transmission: Body fluids
E.g., blood, semen, breast milk, vaginal
secretions
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Time Course of the Progression of
AIDS after HIV Infection
Figure 9.21
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Immune Deficiency: AIDS
AIDS progression:
• Phase I: few weeks to a few years; flu like
symptoms, swollen lymph nodes, chills, fever,
fatigue, body aches. Virus is multiplying, antibodies
are made but ineffective for complete virus removal
• Phase II: within six months to 10 years;
opportunistic infections present, Helper T cells
affected, 5% may not progress to next phase
• Phase III: helper T cells below 200 cells/mm.,
opportunistic infections and /or cancers present,
clinical AIDS, death [victim actually dies from the
secondary infections occurring after their
immune system is destroyed by HIV]
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AIDS Pandemic
• More than 36 million infected with HIV
worldwide
• Most infections in sub-Sahara of Africa
• Increasing spread in Asia and India
• Most often spread by heterosexual contact
outside U.S.
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Safer Sex
• Abstinence
• Reduce number of sexual partners
• Choose sexual partners with low risk behavior
• Avoid high risk sexual partners
• Use latex or polyurethane condoms or barriers
• GET TESTED
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings.
New AIDS Treatments
• Enzyme inhibitors:
• Protease inhibitors:
• Early treatment may delay/prevent clinical
AIDS
• Vaccine: virus mutates rapidly preventing
effective vaccine production at this time
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings.