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VOCABULARY
A. RESISTANCE: body's ability to counteract effects of PATHOGENS

*PATHOGEN: disease-causing agent

B. SUSCEPTIBILITY: lack of resistance

C. TWO RESISTANCE MECHANISMS work together to keep body healthy

1. INNATE (NONSPECIFIC) DEFENSE SYSTEM: responds immediately to protect
body from all Foreign substances

a. first line of defense – prevent pathogen entry
b. second line of defense – destroy pathogens once in body

2. ADAPTIVE (SPECIFIC) DEFENSE SYSTEM = IMMUNE SYSTEM: attacks
specific pathogens assisting the second line of defense once pathogens are in the
body – sometimes called the “third line of defense”

a. humoral (antibody-mediated) immune response
b. cellular (cell – mediated) immune response
FIRST LINE OF DEFENSE = Surface Membrane Barriers (2) preventing pathogen entry
Surface Membrane Barriers (2) preventing pathogen entry

1. MECHANICAL BARRIERS

a. unbroken skin and mucous membranes
1) normal bacteria on skin inhibit new, pathogenic bacteria
2) mucus on membranes traps particles, cilia push bacteria out

b. flush pathogens out by: lacrimation, salivation, urination, defecation, vomiting,
and perspiration

2. CHEMICAL BARRIERS

a. LYSOZYME: in tears, saliva, mucus, sweat: kills bact.

b. SEBUM: oil, and salts in sweat, create an inhospitable environment for bacteria

c. HCL in stomach kills bacteria
SECOND LINE OF DEFENSE = INTERNAL DEFENSES:
Cells And Chemicals: if
pathogens breech surface membrane these mechanisms take over to combat disease
PHAGOCYTES
a. NEUTROPHILS: first to the site of infection -> die after engulfing a few
bacteria increase in number with infection
PUS: accumulation of dead neutrophils, cell parts & bact.

b. MACROPHAGES: monocytes that left blood stream: clear away debris,
bacteria, and invading agents

c. EOSINOPHILS: help protect against parasites
NATURAL KILLER CELLS (NK CELLS):
lg, granular lymphocytes that lyse & kill
cancer & tumor cells, virus-infected cells before the immune system has been enlisted
INFLAMMATION
: tissue response to injury/infection: sets stage for repair. Four signs
of short-term inflammation

a. redness and heat: due to increased blood flow to area: increases metabolism and movement of healing cells

b. swelling (edema): due to increased permeability of bv to fluids

*HELPS DILUTE HARMFUL SUBSTANCES
*brings lots of O2 and nutrients for repair
*allows for clotting proteins to enter area
*neutrophils and monocytes enter to eat up junk
*prevents spread of pathogens

c. pain: due to edema, pressing on nerves

d. impaired function (ie if a joint)
TWO ANTIMICROBIAL PROTEINS
COMPLEMENT & INTERFERON
COMPLEMENT
group of plasma proteins. When activated, help destroy
foreign substances by lysis of bacteria and amplify the inflammatory response
INTERFERON
: produced by virus-infected cells

*cell invaded by virus, virus takes over cell and replicates, filling the cell
with more viruses

*when cell ruptures, many viruses are released and can attack other
healthy cells in the area

*HOWEVER, virus-infected cells release INTERFERONS: IFN's.

*IFN's diffuse to nearby cells, and stimulate protein synthesis which
inhibits or interferes with viral replication in those cells

*IFN's protect these cells from a variety of viruses
FEVER
upward resetting of body temperature in response to PYROGENS secreted by
leukocytes and macrophages during exposure to bacteria/viruses

*dangerous if too high (denature proteins)

*helpful if mild: liver and spleen sequester Fe and Zn which bacteria need to
survive, increases metabolic rate of cells to fight bacteria
ADAPTIVE (SPECIFIC) BODY DEFENSES
IMMUNITY (work with non-specific defenses)
IMMUNE RESPONSE
activity of the immune system, amplifies inflammatory response,
stimulates complement release. Different from the non-specific defenses in three ways:

1. SPECIFICITY OF RESPONSE: antibodies produced by the WBC's seek and destroy
specific "NON-SELF" antigens, while preserving antigens recognized as "SELF"

*AUTOIMMUNE DISEASE: body does not recognize "SELF" and destroys
healthy tissues (scleroderma, rheumatoid arthritis, multiple sclerosis, psoriasis)

2. MEMORY OF IMMUNE SYSTEM: once exposed to an antigen, components of the
specific defense mechanism remember agent & launch a quicker defense in future
exposures

3. RESPONSE OCCURS ALL OVER BODY: not limited to initial area of infection
LYMPHOCYTES: PRIMARY CELLS OF THE IMMUNE SYSTEM
2. T-LYMPHOCYTES (T-CELLS): 70% of immature lymphocytes migrate to thymus, in
presence of thymosin "LEARN" to recognize "SELF" and "NON-SELF" antigens.
These are partially mature T cells.

3. B-LYMPHOCYTES (B-CELLS): 30% of immature lymphocytes partially mature in
the bone marrow or in the liver

4. each partially mature T and B cell is capable of recognizing only one antigen for its
entire life – very specific. The antigen a particular cell will recognize is determined by
our genetic material.

5. both T and B cells are capable of responding to many of the same varieties of antigens
(ie chicken pox virus)

6. partially mature T and B cells migrate to the lymphatic system (nodes, spleen etc.) and
continue to circulate thru body fluids until they meet their specific antigen.

7. once partially mature T and B cells meet their specific antigen, they will complete their
development into fully functional cells.
MACROPHAGES
: ACCESSORY WHITE BLOOD CELLS FOR THE IMMUNE SYSTEM

1. come from monocytes that migrate into tissues

2. ANTIGEN (AG) PRESENTERS: engulf AGs, place signals on their membranes to
notify T-Cells an AG has been phagocytized.


3. secrete chemicals that activate T-cells, T-cells then secrete chemicals that turn the
macrophages into cells that rapidly phagocytize antigens while secreting bactericidal
chemicals.
HUMORAL IMMUNE RESPONSE
(antibody-mediated immunity) B-cells

* best in defending body against:
bacteria
free viruses (not inside of cells, but free in body fluids)
toxins
PRIMARY IMMUNE RESPONSE
occurs upon first exposure to a specific Ag

1. ANTIGEN CHALLENGE: partially mature B cell encounters Ag & is "activated"

2. CLONAL SELECTION: B cell is stimulated to divide producing a colony of B cells
exactly like it (called a CLONE) to combat this specific Ag.

3. PLASMA CELLS: most cells of the CLONE become plasma cells which secrete
ANTIBODIES (= IMMUNOGLOBULINS = IG)for 4-5 dd before dying (this occurs
3-6 dd post exposure)

4. IG's: the gamma globulin part of plasma proteins, bind to antigens, and mark them for
destruction BY NON-SPECIFIC DEFENSE MECHANISMS OR BY T CELLS (peak
levels around 10dd post-exposure then decline)

5. MEMORY CELLS: all other cells of the CLONE become long- living memory cells,
that live to mount stronger, faster attacks against the same antigen in the future
SECONDARY IMMUNE RESPONSE
upon second/subsequent exposure to same Ag

1. faster, longer, more effective response

2. MEMORY CELLS: recognize antigen & stimulate production of PLASMA CELLS to
produce Igs necessary to combat the Ag.(occurs w/in hrs after memory cell exposure)

3. Ig levels rise to a peak within 2-3 dd, higher peak than before. Ig levels remain high
for weeks or months.
ACTIVE HUMORAL IMMUNITY
you are exposed to Ag and your B cells develop
memory cells to combat same Ag in future

a. NATURALLY ACQUIRED AHI: exposed and develop symptoms of
bacterial/viral infection

b. ARTIFICIALLY ACQUIRED AHI: vaccination of dead or weakened Ags
which stimulate B cells to develop Ig - never are sick
PASSIVE HUMORAL IMMUNITY
Ig not made by your body, they are harvested
from another human or from an animal. Temporary immunity, since there are no memory
cells to protect you in the long term.

a. NATURALLY ACQUIRED PHI: fetus receives Ig from mother's blood thru
placenta, babies receive Ig from mother thru breast milk. Lasts for several
months after birth.

b. ARTIFICIALLY ACQUIRED PHI: shot of immune serum (gamma globulins)
that immediately protect body from Ag. Needed if exposed to Ag that would
kill you before you naturally develop a resistance. Effects are short term (2-3
wks)
CELL-MEDIATED IMMUNE RESPONSE
T-cells

* best in defending body against:
INFECTED, ABNORMAL OR FOREIGN CELLS
virus, fungi, protozoan, parasite-infected cells
cancer cells
transplanted cells
ANTIGEN CHALLENGE
T cells exposed to an antigen:
- on a foreign or abnormal cell
- found as an antigen "flag" on an infected "SELF" cell
- on an ANTIGEN PRESENTING CELL (usually macrophages)
ANTIGEN BINDING
A specific T cell recognizes and binds to an Ag & is stimulated
MACROPHAGE + ACTIVATED T-CELL
secrete chemicals to stimulate division of
activated T cells to produce a colony of the same type of T cells. Population of T cells
= a CLONE, which all destroy the specific antigen
T CELLS
are the main cell involved: several types

a. CYTOTOXIC T CELLS or KILLER T CELLS:
1) kill cells infected with: viruses, parasites
2) kill cancer cells
3) kill foreign cells (HAMPERING transfusions, transplants)

b. HELPER T CELLS:

1) WITHOUT THESE CELLS, THERE IS NO IMMUNE RESPONSE:
coordinate, & help complete activation of all other immune cells (T & B)
2) secrete chemicals to promote division of specific B & T cells to
increase the population of cells responding to the antigen

3) Ensure that B cells "notice" the Ag and produce antibodies against it.

4) stimulate increased non-specific defense mechanisms

5) THESE CELLS ARE DESTROYED BY THE AIDS VIRUS


c. SUPPRESSOR T CELLS:

1) RELEASE LYMPHOKINES which suppress T and B cells

2) involved in the "wind down" of an immune response once the antigen
has been inactivated or destroyed
CHAPTER 21: THE IMMUNE SYSTEM: INNATE AND ADAPTIVE BODY DEFENSES
CHAPTER 21: THE IMMUNE SYSTEM: INNATE AND ADAPTIVE BODY DEFENSES