Notes

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DEFENSE MECHANISMS OF THE BODY
INNATE SYSTEM: NON-SPECIFIC DEFENSES
These are considered nonspecific defenses of the body given that they protect the body against
ALL foreign substances.
FIRST LINE OF DEFENSE (EXTERNAL INNATE)
This line of defense includes the external body membranes and skin. The unique features of these
two barriers offers further protection.
BARRIER PROTECTION
skin’s keratin protein
acidic pH
lacrimal glands: tears w/ lysozyme
salivary glands: saliva w/ lysozyme
sebaceous glands: sebum w/ antimicrobial chemicals
respiratory tract: mucociliary escalator created by cilia actions
defecation
urination
vomiting
SECOND LINE OF DEFENSE (INTERNAL INNATE)
This line of defense begins when the first defense has failed. The actions of antimicrobial proteins,
phagocytes and assorted other cells collectively to manage the situation. As a result of these efforts,
the site of penetration begins to exhibit the signs of inflammation. Two categories of actions operate
here - cellular and chemical.
CELLULAR
PHAGOCYTES’ RESPIRATORY BURST: macrophages/monocytes, neutrophils, eisonophils, mast cells
NATURAL KILLER (NK) CELLS: perforins perforate cancer & viral-infection cells, secretes
interleukins (IL) for positive feedback in inflammatory response
INFLAMMATION: initiated by histamine, kinins, prostaglandins, platelet-derived growth factor,
complement proteins, cytokines . . . see flow chart next page for more details
NATURAL FLORA: bacterial (E. coli), fungal (S. Cerevisiae)
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2
CHEMICAL
ANTIMICROBIAL PROTEINS CALLED INTERFERON (IFN): viral-infected cells release IFN which diffused
to it neighbors . . . neighbors (1) produce protein PKR which shuts down protein synthesis at ribosome
in these healthy cells and (2) positive feedback on macrophages & NK
ANTIMICROBIAL PROTEINS CALLED COMPLEMENT: 20 plasma proteins acting in a cascade fashion with
eventually lead to lysis of the infected cell (see photograph below for more details)
HYPOTHALAMIC RESPONSE = Fever: secreted pyrogens trigger reset of thermostat to higher value; this
new temperature results in (1) denaturing pathogen proteins and (2) liver’s sequestering of Fe and Zn
NOTES
<
IFN varies include: gamma (lymphocytes), alpha interferon (other leukocytes), beta interferon
(fibroblasts)
<
IFN directly acts on malignant cancer cells; pharmaceutical IFN available by biotechnology but
are exceedingly cost prohibited to most individuals
<
Alpha IFN used to treat genital warts and hepatitis C
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ADAPTIVE SYSTEM: (SPECIFIC)
THIRD LINE OF DEFENSE: CELL MEDIATED AND ANTIBODY MEDIATED IMMUNITY
How does the body must recognize a foreign substance. This is accomplished by two methods.
<
antigen (Ag) with antigenic determinate sites
<
major histocompatibility complex (MHC I or II) markers
•
MHC I . . . all body cells
•
MHC II . . . immune system cells
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B AND T CELL CHARACTERISTICS COMPARED
T
B
maturation site
thymus
bone marrow
immunity type
cell mediated
antibody mediated
subpopulation
Th, Tc, Tnk
Bp, Bm
no
yes
surface antibodies
CELL MEDIATED IMMUNITY
(1) Phagocytosis of antigen (Ag) by antigen-presenting cell (APC) such as macrophage, PMN.
(2) Antigen presented on the membrane of the APC along with MHC II marker.
(3a) APC with Ag/MHC-II binds via CD4 & T cell receptor (TCR) to the T helper cell producing an
activated T helper cell.
(3b) Antigen-infected cell/MHC-I cell binds with via CD8 & TCR to T cytotoxic cell producing an
activated T cytotoxic cell.
(4a) Activated T helper cells serve in the co-stimulation of humoral (antibody) mediated immunity.
(4b) Activated T cytotoxic cells lead to cellular lysis or phagocytosis.
In both cases, activation of T helpers and T cytotoxic, (1) memory cells are produced with will allow
for a faster response should the same antigen present itself in the future and (2) clones of the specific
T cell in mass produced for a more enhanced response.
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ANTIBODY MEDIATED IMMUNITY (A.K.A. HUMORAL IMMUNITY)
What events(s) trigger an antibody mediated response?
<
correct THelper produces lymphokines which stimulate the correct B cell
<
correct B cell clones are produced
<
B cell binds to the presented antigen
What events lead up to the production of antibodies?
<
correct B cell clones . . . takes about five days to produce antibodies de novo
<
memory and plasma cells produce antibodies by placing them on the cell membrane or secreting
them into the serum
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How does the presence of antibodies on a plasma cell membrane lead to the destruction of the antigen?
<
membrane bound antibodies stimulate the complement cascade which leads to cell lysis or
phagocytosis of the Ag-containing cell
<
serum antibodies bind Ag in an agglutination reaction
I
Is there one kind of antibody? NO! There are several subclasses of antibodies. You should remember that
Ig stands for immunoglobulins. Antibody come in different shapes. The IgG antibody is the typical one
used for antibody structure; this is the one I will use. Please memorize figure 21.2. In addition, you are to
memorize table 21.3 illustrating the detailed difference between the five types of antibodies. The table below
will assist you in extracting the important information from table 21.3.
ANTIBODY
%
CIRCULATING
IgA
15
IgD
1
IgE
0.1
LOCATION
saliva, sweat, intestinal
juice, breast milk
antigen receptor on B cell
surface . . . aid in B cell
activation
75
IgG
IgM
FUNCTION
5-10
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The Th cell is the key player to both the cell mediated and antibody mediated immunities.
There are several means by which immunity can be
conferred. Active immunity is naturally acquired
when you suffer from an bacterial or viral infection.
In contrast, artificially acquired immunity occurs via
vaccinations.
April 6, 2009 (10:47am)
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