Transcript 48-2 Specific Defenses: The Immune System

Chapter 48: Infectious Diseases & Immune System
48-1 Nonspecific Defenses
48-2 Specific Defenses: The Immune System
48-3 AIDS
48-1 Nonspecific Defenses
I. Disease Transmission (Genetic, Environmental, Infectious)
• INFECTIOUS disease RESULTS from pathogenic INVASION of body.
(1) Robert Koch (Nobel Prize Recipient, 1905 for “Koch’s Postulates”)
• German physicist REVEALED process for DETERMINING the CAUSE
(etiology) of a disease.
• Postulate ONE
Suspected pathogen MUST be present in DISEASED animal’s tissues and
NOT in a healthy animal.
• Postulate TWO
Suspected pathogen should be ISOLATED and CULTURED in a laboratory.
• Postulate THREE
A HEALTHY animal inoculated with THIS culture should develop the SAME
disease.
• Postulate FOUR
Pathogen from NEWLY infected animal should be IDENTICAL to
ORIGINAL infected animal when examined.
Critical Thinking
(1) In many cases, NOT all of Koch’s postulates can be applied to determine
the cause of a HUMAN disease. Why might this be?
II. Skin and Mucous Membranes
• FIRST lines of MECHNICAL defense (a tough keratinized shield).
(1) Mucous Membranes (cell linings SECRETE mucus)
• Epithelial tissues PROTECT interiors of body (e.g., LININGS of
digestive, respiratory, and excretory tracts).
(2) Mucus
• Thick, STICKY secretion TRAPS and DISSOLVES pathogens.
III. The Inflammatory Response
• Initiated when DAMAGED cells release CHEMICAL messengers, including
HISTAMINE. (e.g., Results in Swelling, Redness, Warmth, and Pain)
(1) Histamine (released by DAMAGED cells)
• Increase BLOOD FLOW to injury and PERMEABILITY of nearby
capillaries.
(2) Neutrophils (MOST common phagocytes DRAWN close by histamines)
• Circulate through BLOOD and SQUEEZE through a capillary to reach a
marked INFECTION site.
(3) Macrophage (class of phagocytes)
• Consume pathogens, worn out cells, and cellular debris.
(4) Natural Killer Cell (NON-specific leukocyte)
• Patrol body looking for any “foreign” cells AND will puncture membrane,
causing LYSIS (e.g., viral-infected cells, cancer cells).
IV. Other Nonspecific Defenses
• INTERFERON and FEVER; work with skin, mucous membranes, and
inflammatory response to rid NON-SPECIFIC pathogens.
Critical Thinking
(2) Many people take FEVER-REDUCING drugs as soon as their
temperature exceeds 99 degrees F. Why might it NOT be a good idea to
immediately reduce a fever with drugs? On the other hand, what may be
the BENEFITS of taking fever-reducing drugs?
(1) Interferon (protein/CYTOKINE produced by INFECTED body cells)
• WARNING SIGNAL that alerts nearby cells to make and release
ENZYMES to INHIBIT viral production.
(2) Fever (chemically-induced by macrophage “smoke signals”)
• Brain told to ELEVATE metabolism  results in HIGH body temperature.
GOAL: To stimulate the immunoresponse (WBC activity) and/or SUPPRESS
the growth of some BACTERIAL/VIRAL infections.
48-2 Specific Defenses: The Immune System
I. The Immune System (leukocytes, lymphocytes, and antibodies)
• Includes bone marrow, THYMUS gland, lymphatic system, and SPLEEN.
(1) Thymus (GLAND located above heart)
• T cells made in bone marrow BUT develop and mature in thymus gland.
(2) Spleen
• Stocked with LEUKOCYTES to FILTER pathogens in bloodstream.
(3) B cells (lymphocyte; produced AND mature in bone marrow)
• Can be activated by ANTIGENS to make and release ANTIBODIES.
(4) T cells (lymphocyte; MADE in bone marrow BUT matures in THYMUS)
3 types
(1) Helper T Cell
(2) Cytotoxic T Cell
(3) Suppressor T cells
II. Recognizing Pathogens (SPECIFIC DEFENSE)
• Lymphocytes respond WHEN antigen is recognized as FOREIGN (non-self).
Critical Thinking
(4) Virologists have created an effective vaccine for smallpox, BUT have
not been able to do so for HIV. What does this suggest about the rate of
evolution of the smallpox virus?
(1) Immune Response (TWO methods of DEFENSE)
• A 2-way assault on a PATHOGEN:
(1) Cell-mediated
(2) Humoral
(2) Antigen (a protein OR glycoprotein, often on CELL SURFACE)
• Includes pathogen, PARTS of pathogen, toxins, insect venom, & POLLEN.
III. Immune Response (HOW one is ELICITED)
• Pathogen  Macrophage  APC—Interleukin-1  Helper T Cell —IL-2 
Cytotoxic & Suppressor T Cells [interleukins = cytokines]
(1) Cell-Mediated Immunoresponse (CMI, NO antibodies YET)
• 1st arm of DEFENSE  Cytotoxic T-cell attack on a PATHOGEN.
Critical Thinking
(5) Cytotoxic T cells attack and destroy some kinds of CANCER cells.
What can you conclude about the surface proteins of these cancer cells?
(2) Humoral Immunoresponse (HMI)
• 2nd arm of DEFENSE  B cells and ANTIBODIES.
(3) Helper T Cell (activates BOTH cytotoxic T cells AND B cells)
• Coordinates BOTH methods of immunoresponse against an antigen.
(A) Cell-Mediated Immunoresponse (1st Arm)
• IL-2 (Helper T Cell) stimulates Cytotoxic T cells and Suppressor T cells
to rapidly divide.
(1) Cytotoxic T Cell (antigen-SPECIFIC lymphocyte)
• Programmed to destroy ONLY cells with antigens that MATCH its
receptors
(i.e., only specifically INFECTED cells)
(2) Suppressor T Cell (signals to B cells to STOP making antibodies)
•SHUTS DOWN immunoresponse ONCE pathogen is CLEARED from body.
(B) Humoral Immunoresponse (2nd Arm)
• IL-2 and APC stimulates B cell to DIVIDE into ANTIBODY-making
“PLASMA CELLS.”
(1) Plasma Cells
• Activated B cells release ANTIGEN-SPECIFIC antibodies into blood.
(2) Antibodies (30,000 released per SECOND, immobilizers)
• Tiny, Y-shaped sticky PROTEINS attach to antigens ~ immobilization.
(C) Primary and Secondary Immune Response
• AFTER infection, immuneresponse is SHUT DOWN and MOST cells die.
Critical Thinking
(6) A friend tells you that because he has JUST recovered from a cold, he
now cannot get the flu. Is your friend right? Explain.
(1) Memory Cells (how you ACQUIRE immunity)
• Long-term B and T cells patrol body for YEARS; if pathogen ENTERS,
they quickly divide and wipe it out BEFORE symptoms appear.
(2) Primary Immune Response
• 1st time body encounters an antigen (SLOWER than a secondary response,
antigen is NEW).
(3) Secondary Immune Response
• A 2nd infection caused by SAME pathogen,  MUCH FASTER and MORE
POWERFUL immunoresponse.
(LOTS of antibodies made quickly)
IV. Immunity (passive & active) and Vaccination
• A VACCINE prepares immune system to RECOGNIZE a pathogen should it
REAPPEAR in its disease-causing (virulent) form.
(1) Immunity (i.e., resistance to pathogens)
• Immunity is ACQUIRED through exposure (to a pathogen) through
sickness OR vaccination. (GOAL: To produce those Memory B and T cells)
V. Allergies (e.g., ALLERGENS can be pollen, food, mold spores, venom)
• WBCs attack a HARMLESS antigen,  symptoms associated with release
of HISTAMINE
(i.e., watery eyes, sneezing, wheezing))
VI. Autoimmune Disease (e.g., MS, Lupus, Type 1 diabetes, Arthritis)
• WBCs mistakenly recognize SELF tissue as FOREIGN, and attack healthy
body tissues AS IF they WERE pathogenic.
48-3 AIDS
I. HIV and AIDS
• HIV (a retrovirus) may invade several types of WBCs, BUT targets
Helper T Cells via a CD-4 receptor.
Critical Thinking
(6) The Center for Disease Control (CDC) is reviewing TWO proposals for
HIV research, BUT it can fund only ONE. Suppose you are asked to
provide input. Which proposal would you recommend the CDC fund?
(NOTE: considering effectiveness and potential adverse side effects)
Proposal One: Develop a drug that interferes with protein synthesis.
Proposal Two: Develop a drug that binds to CD4 receptors on helper T
cells.
(A) Course of the Disease
• As helper T cells falls, immunity weakens, opening up for opportunistic
infections.
(1) Opportunistic Infections (when T cell count drops below 200/mL)
• Include cancers, pneumonia, influenza, and usually strike people with a
compromised immune system (normal T cell count ~ 600-700/mL blood)
(B) Transmission (intercourse, non-sterilized syringes)
• Body fluids containing HIV or HIV-infected cells.
(C) Treatment and Vaccines
• HIV genes mutate frequently; NO current cure for HIV although
experimental vaccines AND antiviral drugs are being explored.