PLEASE CHOOSE FROM THE

FOLLOWING TOPICS:
 The OBJECTIVES for this report include the following:

3. To be able to describe the hematopoietic system.

4. To be able to identify and describe the types of responses of the
body to infection and foreign bodies.
5. To be able to present new discoveries and breakthroughs about
the defenses of the hematopoietic system.
Overview/Description of the Hematopoietic
System

“hematopoietic”

haima - “blood” (Greek) poiein - “to make”

•blood-making processes
•differentiate and proliferate specific stem cell progenitors
to produce the various mature cell forms.
•Two types of blood-forming or hematopoietic tissue:
• myeloid tissue
• lymphoid tissue
 B Lymphocytes

Erythroid
Erythrocytes
CFU
Self-renewing
stem cell

Megakaryocyte
Platelets T Lymphocytes
Pluripotent
stem cell
Lymphoid
Granulocyte-monocyte
Neutrophils Monocyte progenitor
Basophil
Basophils
MyeloidCFU CFU
progenitor Natural killer (nk)
Eosinophil
Eosinophils cells
CFU
The organs of the hematopoietic system are positioned
throughout the body - called lymphoid organs (home to
lymphocytes)
 Definition of Terms
• Hematopoietic vs. Immune and Lymphatic System
- very much related
- all works for the defense mechanism of the body.
• Infection
- detrimental colonization of a host organism by a foreign
species
- Pathogen (infecting organism), interferes with
the normal functioning of the host
• Foreign Bodies
- particularly microorganisms like bacteria and viruses
that may infect the body.
• Innate Response/Non-specific response
- all the mechanisms that defend an organism against a
foreign body regardless of what it is
- present since birth.
 • Acquired Response/Specific response
- basis of this response lies in the capacity of the cells to
distinguish between proteins produced by the body's own
cells and proteins produced by invaders or cells under control of
a virus - has memory
Passive Response
- results when antibodies are produced by one individual and
then acquired by another
- the passive acquisition of an immune response that was
actively acquired by another individual
- last for at most months since antibodies have a finite life span
whereas active immunity (ironically) requires time (days, weeks)
before a functional immune response develops.
 Innate Responses of the Body
Against Foreign Bodies and Infection
First Line of Defense

mucous membranes
skin of nose and throat
tears tiny hairs in the nose

bleeding urinating sweating

 Inflammatory Response

• If the first line of defense was unable to get rid of the invader, the
innate system will trigger an inflammatory response in an attempt
to wall off the intruder and stop its spread
- initiated by pathogens that “turn on” the body’s defenses

• Phagocytes migrate to the site of invasion, activated and begin their

task of digesting and destroying the invading bacteria.
- produce other cytokines that further activate other cells of the
immune system
Interleukin-5 List of TChemical
cells Signals Produced
Induces differentiation of B
cells, and activates some
Microphages
Interleukin-6 Cytokines involved
T cells, Macrophages Costimulator
in the Inflammatory Responseof T cells,
induces growth in B cells
Transforming Growth
Interleukin-10 TT cells, Macrophages
cells Inhibits TBcell
Activates growth
cells and and
Factor Cytokine Producing cell Macrophage
inhibits Action
activation
Macrophage
Interleukin-1
Lymphotoxin Macrophages
T cells function
Stimulation of various
Similar to TNF, cells,
activates
Interleukin-12 Macrophages e.g. T cells,
Microphages
Activates acts and
T cells to initiate
NK
inflammation,
cells induces
Histamine Mast cells Not actually a cytokine,
hypothalamus to increase
Interleukin-13 T cells but an important
Induces chemical
proliferation of B
body temperature
mediator that induces
cells and differentiation of T
Interleukin-2 T cells Causes proliferation
blood vessel
cells dilationofand
activated
increasesTcell
andwall
B cells,
Gamma-Interferon T cells, NK cells Activates
induces Macrophages
antibody synthesis
permeability
Tumor Necrosis Factor
Interleukin-3 Macrophages
T cells Causes
Induces activation
growth and of some
Microphages.
differentiation Induces
of immune
inflammation
cells in bone and
marrowfever.
Induces catabolism of
Interleukin-4 T cells Promotes
muscle andB fat,
cellthus
growth
and differentiation
leading to cachexia (bodily
wasting)
• Primary effect of the inflammatory response: blood circulation to
• Two increase around
ways in which the can
cells affected
commit area through vessel dilation
Apoptosis:
• •TheContinues
immune
- immune until
system infection
presence is done
cells,isonce activated,through
strengthened are primed to commit
the increased
• Phagocytes
Apoptosis blood flow continue to consume and destroy microbes
: Receiving an Apoptosis signal
• Acquired immune system binds and disposes harmful toxins.
- When a chemical signal is received that indicates that
• •HelperPusTisin
Increase produced
cells
body emit thean
heat: stay-alive signal, and keep emitting the
antimicrobial
the cell should kill itself, it does soeffect giving the human
signal forbody - debris/left
as long as theyhand
an upper overs of theand
recognize pathogen
sense foreign antigens
in the body - -prolonging
color of the pus depends
inflammatory on the pathogen
response
: Not receiving a "stay-alive" signal
• Main symptoms of an inflammatory response:
- Certain cells, once they reach an activated state,
• •OnlyHow when
-are dothe
tissues inflammatory
ininfection
the area: responses
hasredbeen end?
and eradicated,
warm and there is no more
programmed to kill themselves automatically
foreign antigen
-within
tissuesthat theKey
in the
a certain area:element
helper
period
T cells- "Apoptosis“
swollen stop emitting the stay-
of time, unless instructed
alive
signal, thus allowing
-otherwise.
area the cells involved
of inflammation: painfulin the inflammatory response
• off.
to die Necrotic death: cells die in a normal fashion
- There may be other cells that supply them with a
• •Inflammation:
Cells can be killed incaused
response another way: by destroying themselves
"stay-alive" signal - delaysby themicrobial
Apoptosisinfections, physical
- Apoptotic
agents, death resulting from inadequate blood
tissue necrosis
• flow and radiation.
- may result into: redness, heat, swelling and pain.
 Interferons

• Interferon: a group of proteins produced by the white blood

cells (alpha and beta interferon production) and activated
T-cells (gamma interferon production) in response to an
attack by a virus.
- Prevents the entry of a virus into cell by attaching
themselves to neighboring cells, prompting to start
producing their own protective antiviral enzymes -
limiting the amount of new cells that become infected.
- Result: impairment of the growth and replication of
the attacking virus.
• stimulates the production of cytokines that activate
macrophages, natural killer (NK) cells, and cytotoxic T-
lymphocytes (CTLs, or killer T-cells)

• 1957: discovery of the antiviral properties of interferon

• 1978: further research developed 10 purified interferon proteins
• 1981: first genetically re-engineered interferon injected into a
human
• 1986: first interferon to treat leukemia was approved by the FDA

• Interferon: also approved to treat many other diseases

The figure shows a re-engineered interferon. Comparison of the surfaces of
- Cancer
wildtype Interferon-beta (left) and the soluble variant with reduced
- Hepatitis
hydrophobicity B engineered at Fraunhofer IGB(a possible cure for
(right)
- Kaposi’s
multiple sclerosis).sarcoma
Arrows indicate regions of substitution. Hydrophobic
- Hepatitis C are blue, hydrophilic ones are red.
regions
 ***INTERFERON BREAKTROUGH***
Interferon and it’s relationship with down syndrome
CONCLUSION:
Side effects of interferon therapy (given for cancer) are also features
•seenDr.in Leonard Maroun (DS):
Down syndrome of Illinois: noted this fact and has been
working on this topic for the last 20 years
Interferon side effects: neurotoxicity, memory loss, frontal lobe
PROBLEM: To determine the relationship of Interferon
encephalopathy
DS: learning difficulties, and small Down
frontalSyndrome
lobes
Interferon side effects: cardiotoxicity
THEORY:
DS: heart defects
7. Interferon
Interferon could behypothyroidism
side effects: involved in the physical features and
development
DS: hypothyroidismof the child with Down Syndrome.
Interferon- side
exposure
effects:to interferon
autoimmune in the womb may cause an
disease
increased effect via
DS: autoimmune growth inhibition of cells on the fetus.
disease
Interferon side effects: deafness
2. An increase
DS: hearing in the incidence
loss (mostly conductive of but
infectious hepatitis (HepA) was
some neuronal)
Interferonfollowed nine months
side effects: later by an increase in the number of
growth inhibition
DS: shortbirths
stature of babies with DS
- If a woman over 35 years of age had an oocyte sensitive to
PRESENT interferon,
DEVELOPMENT:the interferon could produce non-disjunction in
Meiogen the oocyte,
Biotech: leadingintoorder
company trisomy 21.
to develop an anti-interferon
("Antiferon") drug for testing purposes
 Complement System

• A biochemical cascade of responses that helps clear pathogens

from an organism
- derived from the eleven small plasma proteins produced by
the hepatocytes of the liver - work together to form the primary end result
of cytolysis by disrupting the target cell's plasma membrane.
• Plasma proteins: inactive without infection

• Two pathways complement activation is initiated:

: classical pathway
- activated by antibody-antigen complexes

: alternative pathway
- initiated when a previously activated complement component
binds to the surface of a pathogen, where it is protected
 Biological effects of the Complement System:
1. Opsonisation
- opsonins (particular plasma proteins such as C3b
and C4b) coat foreign organisms either by alternative
3. Lysis pathway or those already bound by antibody
- C5b- binds
greatly enhances
and their
recruits C6 and phagocytosis
C7 to the targetby surface.
means of
binding to specific
- C7 and subsequently complement
C8 change receptors
conformation on red
to expose
hydrophobicblood cells which
domains which insert
transport thelipid
in the complexes
bilayer. to the liver
and spleen
- C5b678 complex where the
catalyses theypolymerisation
give the complexes
of the up
finalto
componentphagocytes for destruction.
C9 which forms a transmembrane pore of ~ 10nm
diameter causing lysis of the cell - macromolecular assembly I
2. Inflammation
s known as the Membrane Attack Complex (MAC).
- The C5a and less potently, the C4a and C3a fragments:
important inflammatory activators inducing vascular
permeability, recruitment and activation of
phagocytes.
 Natural Killer Cells

• Natural killer (NK) cells: constitute a major component of

the innate response system
- attack cells that have been infected by
microbes, but not microbes themselves
- the mechanism of how the NK cells recognize
the infected cells remain unclear
- named "natural killer" : they do not require
activation in order to kill cells

Natural Killer Cells in Blood

• Cytotoxic; small granules in their cytoplasm contain special proteins
such as perforin ***NKand proteases known as granzymes
Cell Studies***
- upon release in close proximity of a cell to be killed, perforin
forms
• Salk pores
and in cell membrane
Pasteur of target cell:
teams discovered granzymes
that when and tyrosine
the receptor
associated
kinasesmolecules
are missing,cannatural
enter -killer
induce apoptosis
cells are still armed with their
• arsenal
Distinction between and
of enzymes apoptosis andbut
cytokines cellthey
lysis: lysing
can't a virus-infected
dip into their
weaponscell cache
wouldbecause
– releasingthey of virions;
lack the fullapoptosis
spectrum of - destruction
surface of
the virus
molecules inside
that gives them the "license to kill.“
• -NK cells: Activated
receptor in response
tyrosine kinases to interferons
normally receive signals or macrophage-
from a cell's
derived cytokines
environment and, upon activation, add a phosphate group to
- serveproteins,
intracellular to contain viral infections
initiating while adaptive
a new repertoire immune
of cellular behaviors.
response
Thus, isthegenerating
discovery antigen-specific cytotoxickinases
of Receptor tyrosine T cells that
nowcanmakes the
clear the infection.
mechanism of the NK cells more clear.
• Patients deficient in NK cells prove to be highly susceptible to
early phases of herpes virus infection.
This includes T and B lymphocytes and can be divided into cellular and
humoral responses.

Cellular immune response = is mediated primarily by T cells and

limits intracellular infections by organisms such as viruses, parasites
and mycobacteria.

Humoral Immunity = is the aspect of immunity that is mediated by

secreted antibodies, produced in the cells of the B lymphocyte lineage
(B cell). Secreted antibodies bind to antigens on the surfaces of
invading microbes (such as viruses or bacteria), which flags them for
destruction.

*T lymphocyte and B lymphocyte responses are not independent of one another

 IgG2 11-15 21-24 Pathogen neutralization in tissues

Humoral Immunity
Pathogen neutralization in tissues
Properties Of Human Antibody Isotypes
IgG3 Classical complement activation
%0.03-0.06
of total Ig Biological
7-8
Isotype Biological Functions
Opsonization
(adult serum) half-life (days)
NK cell ADCC
IgA1 11-14 5.9 Transplacental
Pathogen transferin
neutralization
IgA2 1-4 4.5 mucosal secretions
IgD 0.2 2-8 Membrane BCR
IgE 0.004 1-5 Pathogen neutralization
Mast cell in tissues
histamine release
IgG4 0.015-0.045 21-24 Pathogen neutralization in tissues
Transplacental transfer
IgG1 Classical complement activation
45-53 21-24
Opsonization
ClassicalNK cell ADCCactivation
complement
IgM 10 5-10 Transplacental transfer
Membrane BCR (monomer)
 Primary Immunodeficiencies
Disorders of Humoral Immunity
•• Primary immunodeficiencies
Disorders include
of humoral immunity affectaBvariety of disorders and
cell differentiation that
render patients
antibody Laboratory
more susceptible
production. Testing
to infections.
Collectively, these disorders account for
approximately 50% of primary immunodeficiencies.
• Common primary immunodeficiencies include:
• complete blood
of cell count
Subgroup Onset (CBC) with manual
Pattern of differential,
Other features
- disorders humoral immunity (affecting
infection B-cell differentiation
quantitative immunoglobulin
or antibody production), measurements (IgG, IgM, IgA),
• Disorders of
measurements After
of 6 months antibodies
functional Encapsulated
against Reccurent
immunized antigens,
- T-cell
humoral defects and combined
of age; can B- and
bacteria: T- cell defects,
infections: sinus
• immunity
delayed type hypersensitivity skin tests.
- phagocytic
(B cell disorders
present in Haemophilus infections,
differentiation
- complementadulthood
deficiencies. infleunzae, pulmonary
• andTheantibody
CBC with manual differential can detect deficiencies
pneumococci, infections in immune
production)
cells and platelets. In most streptococci
instances, Chronic
a normal CBC
• Major indications of this disorders include:
Fungi and gastrointestinal
eliminates the diagnosis
- multiple infectionsof T cell defects
parasiteor combined
tractBproblems,
cell and T
cell defects. Virus:
- infections with unusual opportunistic including
organisms
enterovirus malabsorption
- failure to thrive or poor growth(especially with
- positive family history X-linked
agammaglobulin
emia)
 Nonspecific Cellular Components
Cell-Mediated Immunity
5.
1.After the TH cellthat
Macrophages bindsaretostimulated
an antigen-MHC target on
by ingesting anan APC, IL-1
antigen or by
1. cytokines activates
The cell-mediated
become
Typestheactivated
THcell
immune to to
secrete
system
of T Lymphocytes the cytokine
depends
have enhanced
(T on
Cells) IL-2.
T The
cells
phagocytic (T-IL-2
ability.
lymphocytes) bindsand
2. Natural to other
killerdoes(NK)receptors
notcells
involve on
lyse the same
antibody THand
celltumor
production.
viral-infected causing it to
cells.
1.2.T cells: proliferate
Cellular immunity
classified and
Cellular
according differentiate
is primarily
Components
to their into
a response a clone
toand
of Immunity
functions of matureviruses,
intracellular
cell-surfaceTH cells
multicellular
receptors, specific
parasites,
called CDs for(clusters
that antigen.
transplanted Only TH
tissue, andcells
of differentiation). cancerthatcells.
have been
T The
1. Antigen
2. Interrelation
stimulated
cellsmust
are responsible byofan
be processed Cell-Mediated
forantigen haveand
cell-mediated
by Humoral
receptors
immunity.
an antigen-presenting Immunity
for IL-2
cell and
(APC) thusand
these THon
2. Afterpositioned
differentiation cellsinare
the thespecific
surfacethymus for
of the only that
gland,
APC stimulatory
T cells
next migrate
to an MHCto antigen.
marker.
1. TH cells
lymphoid
3. The major activate
Production
tissue. B of
cells
IL-2toand
histocompatibility produce antibodies
other cytokines
complex (MHC)by against
these T-dependent
consists TH cells
of cell-surface
3. TT cellsantigens
Cellsstimulates (usually
differentiate
proteinsand that other
Cell-Mediated
areinto protein
cells of
effector
unique in
to the composition).
Immunity
T
each cell-mediated
cells when and
individual (e.g.,
they areTC cells)
self and
stimulated
indicate by
2. Antigens
molecules. that
anhumoral directly
antigen. (e.g., activate
B cells)Bimmune
cells aresystems.
called T-independent
antigens
Some(usually polysaccharide cellsin composition).
•3. 6.
4. Cytotoxic
Helper (TH)T cells
Teffector (TC) or
T cells CD8
(alsobecome
known release
memory
as perforin to lyse and
cells.recognize
CD4 cells) cellsbind to
Cell-mediated
In antibody-dependent immunity involves
cell-mediated cytotoxicity (ADCC), NK cells,
an carrying
antigen the
in target antigenwith
association andan MHC.
MHC on the surface of an
specialized lymphocytesand
macrophages, called
otherT cells
leukocytes (T-
lyse antibody-coated cells
APC7. Delayed hypersensitivity
causing thewhichAPCrespond
to secrete TD cells are
the cytokine associated
IL-1. with certain
lymphocytes),
that are tootypes
large of
to allergic
be phagocytosed. to
reactions and transplant rejection.
intracellular
4. 8.
ADCC is useful TS antigens.
against
Suppressor cellshelminthic
appear to parasites
regulate the andimmune
protozoans.
response.
 Allergies

• Allergies: Type I Hypersensitivity

• Hypersensitivity: results from damage done to the body by an
immune response.
- Classified into four types based on mechanism of tissue
damage:Type I, Type II, Type III and Type IV Hypersensitivity.
Type I (immediate) hypersensitivity: mediated by IgE and mast cells.
• IgE-mediated allergic reactions include: hay fever, skin inflammation
•• Children
Vaccinations,
(urticaria),
earlywith
are born useaof antibiotics, the
predominant
food allergies, asthma,Th2
use of pasteurized
andcytokine
systemic profile. milk the
Within
anaphylaxis
instead
first of unpasteurized
5 years ofalife, and milkprobably
most (teeminginwith
the micro-organisms),
firstlinked
two years of
• Risk of developing Type I hypersensitivity (atopy): to family
life, immune anddeviation
an industrialized lifestyle with less children result insubjectsless
history and IgE levels occurs resulting in the majority of
developing exposure
a more to infectious
balanced agentscytokine
and less stimulation of the
• New studies have tried toTh1/Th2
prove the response
idea that that there has been an
immune
• Originincrease system to
of this Hygiene release interleukin-12 and interferon
in atopyHypothesis:
and allergic Strachan
diseases in 1989
over thewhere
last 30heyears
studied gamma, botheczema
needed in to 17,414
stimulate a Th1 cytokine response
(allergichay feveratopic
rhinitis, and asthma, and atopicBritish school
dermatitis) children
that from
Hygiene
birth with
to 23 years simultaneous
of age suppression of the Th2 cytokine response -
Hypothesis may be one of the main reasons behind the increase.
• Hygiene -immune
findings deviation
showed
Hypothesis:
or the Th2 response
prevalence
idea that thereofisboth
remains
allergic
an increase
predominant
rhinitis and
in world-wide
eczema with atopy
were reduced andasa number
predisposition
of oldertoward theindevelopment
siblings household of
allergic disease, more marked in developed countries, that is
increase, allergic diseases.
secondaryresults were
to a lack of independent
many viral and of bacterial
the socialinfections
stature ofthat the father
used to
•occurThe increase in family
in the first two years of lifesize led to increased number of infections that
• reduced expression of diseases studied - “sibling effect”
 List of Some Vaccines/Immunizations
Hepatitis B #1 -- Birth (may be delayed for up to 2 months if mother is HBsAg(-)
Hepatitis B #2 -- 1 to 4 months
Hepatitis B #3 -- 6 to 18 months
Diphtheria, Tetanus, acellular Pertussis (DTaP) #1 -- 2 months
DTaP #2 -- 4 months
DTaP #3 -- 6 months
Passive Immunity
DTaP #4 • -- 15Most vaccines need to be updated and/or renewed
to 18 months
DTaP #5 -- 4 to 6 years
• •Active
Tetanus There
Booster immune
-- 11are response:
to 12certain
years made to antigen
recommended vaccinesexposure, either naturally
if traveling
• Special
H. influenzae acquired
type b (Hib) #1during
vaccines infection
are
-- 2 months providedor artificially
to certainacquired by vaccination
racial groups, etc - more
Hib #2 -- 4 months
• #3 Passive
Hib prone
-- 6 months immunity:
to a disease acquired from another individual in the form of
antibodies
Hib #4•-- 12 to
Vaccines:
15 months to stimulate the immune system to protect against
Inactivated Polio #1 -- 2 months
• Passive
microorganisms;
Inactivated Polio #2 immunity:
months protects as
-- 4 microorganisms soon as thealthough
themselves, antibodies are transferred
severely
compromised
Inactivated but#3lasts
Polio so to only
-- 6 as 18not weeks-months
to suffer the fullasbrunt
months the transferred
of the true antibodies are
Inactivated Polio #4 -- 4 to 6 years
removed
sickness/disease
Measles from
, mumps, and the circulation
itself
rubella (MMR) #1 --in 12 ato natural
15 monthsprocess called
“turnover"
MMR • -- 4 Naturally
#2 to 6 years acquired passive immunity: pregnancy
Varicella Zoster Virus Vaccine (chickenpox) -- 12 to 18 months
• •TwoImmunologic
Pneumococcal kinds:
conjugate naturally
vaccine and
tolerance
#1 artificially
for foreign
-- 2 months acquired
antigenspassive
can be immunity
induced
• Artificially
experimentally:
Pneumococcal acquired
conjugate by vaccine
creating passive immunity:
#2 --conditions
4 months short-term
of high-zone immunization
tolerance or by the
Pneumoccocal conjugate vaccine #3 -- 6 months
low-zone
Pneumococcal injection
tolerance of antibodies,
conjugate vaccine such as gamma globulin, that are not
#4 -- 12-15 months
produced
Hepatitis A #1 --by the or
2 years recipient's
older (in selectedcells.areas/situations)
Hepatitis A #2 -- 6-12 months after Hepatitis A #1 (in selected areas/situations)
- mostforcommon
Influenza -- Annually children older way: than immunizations
6 months with certain risk factors. May also be given to all
others wishing immunity. Children under 9 receiving influenza immunization for the first time require 2
doses, 4 weeks apart.
Meningococcal vaccine-- 2 years or older in high risk groups including college students living in
dormitories and military recruits.
 Hematopoietic Response to Infection & Foreign
Bodies

Innate/Non-specific
Acquired/Adaptive Response
Response

Cell-
Humoral Passive
Inflammation Interferon Complement mediated
NK Cells
System
Antibodies
Production Distinct Activated T-
Release of Inactive produced
lymphocytes immunity resulting 
of protein group of
histamine by plasma by B- from the injection 
by WBC and lymphocy
BASOPHILS proteins of lymphocyte of antibodies or 
Lymphocyte tes with
the blood s sensitized 
s no Activation of B- lymphocytes from 
memory cells and another organism
Phagocytosis macrophages;
Protection
and walling Destroys foreign kills virus-
of other Lysis of
of inflamed cells by infected cells
uninfected the
area phagocytosis or
cells infected
cell lysis
http://reach.ucf.edu/~OncEduc1/PDF/sec8.pdf
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES NATIONAL INSTITUTES OF HEALTH
NIH Publication No. 03-5423 September 2003 Guys, sira ung
www.niaid.nih.gov hyperlink ng
www.nci.nih.gov
American Museum of Natural History conclusion sa
http://www.amnh.org/nationalcenter/infection/03_inf/03_inf.html may gilid, kaya
"Immunity's Early-Warning System," Luke A.J. O'Neill, Scientific American, January 2005
Wikipedia Encyclopedia dito kayo
Maroun LE, Heffernan TN, Hallam DM. napupunta.
Department of Medical Microbiology and Immunology, Southern Illinois University School of Medicine
J Interferon Cytokine Res. Feb;20(2):197-203, 2000. Try nyo
Dr G.J.A. Speijers and Mrs M.E. van Apeldoorn pindutin yung
National Institute of Public Health and Environmental Protection
Laboratory for Toxicology sa menu.
Bilthoven, The Netherlands -Oneal
http://www.inchem.org/documents/jecfa/jecmono/v30je04.htm
The National Multiple Sclerosis Information Sourcebook
http://www.nationalmssociety.org/Sourcebook-Interferons.asp
•hcspFACTsheet• A publication of the Hepatitis C Support Project
http://www.hcvadvocate.org/hepatitis/factsheets_pdf/interferon.pdf#search='production%20of%20interferon'
www.sciencedaily.com
The Hygiene Hypothesis and the Primary Prevention of Allergic Diseases
(http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijaai/vol3n2/hygiene.xml)
Immunology - http://microvet.arizona.edu/Courses/MIC419/tutorials.html
The Inflammatory Response - http://alan.kennedy.name/crohns/primer/inflresp.htm
Active and Passive Response - http://www.infoplease.com/ce6/sci/A0858765.html
Created by:
Recommended Vaccination Schedule - http://www.drgreene.com/21_203.html
TM
Basic Principles of Specific Immunity and Immunization - http://www.mansfield.ohio-state.edu/~sabedon/black17.htm