Human Defenses
Microbiology and Parasitology
Non-Specific Mechanism
of Humand Body Defense
Innate Immunity System
Basophil (Granulocyte) - Releases histamines that
cause inflammation.
Eosinophil (Granulocyte) - Kills paradite with
oxidative burst.
Mast Cell (Granulocyte) - Anti-gen presenting cells;
produce antibacterial peptides.
Adaptive Immunity System
, (
Plasma Cell B Cell Lymphocyte ) - Recognizes
antigens and produces antibodies.
(
T Cells Lymphocyte ) - Th cells secrete cytokines.
CTLs| recognize and kill specific nonself cells. Treg
cells are CD4 cells that destroy cells that do not
correctly recognize self cells.
Both Innate & Adaptive Immunity System
(
Neutrophil Granulocyte )- Phagocytizes bacteria
.
and fungi
(
Monocyte Agranulocyte )- Precursor to
.
macrophages Some macrophages are fixed in
certain organs while others wander tissues ,
causing inflammation .
Both Innate & Adaptive Immunity System
(
Dendritic Cell Agranulocyte )- ,
In skin respiratory ,
,
and intestinal mucosa phagocytizes bacteria and
present antigens to T cells .
Natural Killer Cells -(
Agranulocyte )- Kills cancer
-
cells and virus infected cells .
The body’s first line of
defence
The body’s first line of defence
The First-line defenses keep pathogens on the
outside or neutralize them before infection
begins. The skin, mucous membranes, and certain
antimicrobial substances are part of these
defenses.
What is the function of keratin
in the epidermis?
The dermis is the thick inner layer of skin made of
connective tissue.
The epidermis is the thin outer layer, tightly
packed with epithelial cells.
Its top layer is dead and contains keratin, a
protective protein. Shedding of the epidermis
and skin dryness help prevent microbial growth.
Physical Factors
Skin - Acts as a physical barrier; the largest organ
by surface area.
Mucous Membranes:
Epithelial layers secrete mucus (a viscous
glycoprotein).
Mucus keeps surfaces moist and traps
microbes.
Some pathogens (e.g., Treponema pallidum) can
penetrate if mucus barriers are weakened.
Physical Factors
Lacrimal Apparatus (Eyes):
Produces and drains tears.
Blinking spreads tears to wash away microbes.
Excessive tearing flushes out irritants and pathogens.
Saliva:
Produced by salivary glands.
Dilutes and washes away microbes from the mouth and teeth.
Prevents microbial colonization.
Interaction between Microbe
and Host
(
Lacrimal Apparatus Eyes ): Respiratory Tract :
Mucus traps microbes .
Tears wash away microbes from
Nose hairs filter larger particles (>10 µ ).
m
the surface of the eye .
Tears drain through the lacrimal :
Ciliary Escalator Cilia move trapped microbes
canals and nasolacrimal duct into
upward toward the throat .
.
.
Coughing and sneezing help remove microbes
the nose
Epiglottis covers the larynx during swallowing to
block microbes from entering lungs .
Interaction between Microbe
and Host
Ear Defense:
Digestive Tract:
Hairs and earwax (cerumen) trap and
Peristalsis moves contents through the
block microbes, dust, and insects.
GI tract.
Genitourinary Tract:
Defecation, vomiting, and diarrhea
Urine flow cleanses the urethra and
expel harmful microbes.
prevents infection.
Vaginal secretions remove microbes.
Normal Microbiota and Innate
Immunity
Normal Microbiota:
Microbes that permanently live in and on the body
without causing disease. Not officially part of
innate immunity, but they offer important
protection.
Normal Microbiota and Innate
Immunity
Competitive Exclusion:
Compete with pathogens for space and
nutrients.
Effective against Clostridium difficile,
Salmonella, Shigella, and Candida albicans.
Normal Microbiota and Innate
Immunity
Immune System Development:
Normal microbiota are essential for immune
system maturation, even before birth.
Second Line of Defense
The Inflammatory
Response:
A Complex Concert of
Reactions to Injury
The inflammatory response is a
powerful defensive reaction, a means
for the body to maintain stability and
restore itself after an injury. But when
it is chronic, it has the potential to
actually cause tissue injury,
destruction, and disease.
Stages Of Inflammation
Phagocytosis:
Ingestion and Destruction
by White Blood Cells
By any standard, a phagocyte
represents an impressive piece of liv
ing machinery, meandering through
the tissues to seek, capture, and
destroy a target.
Interferon: Signaling for
Viral Defense and Immune
Modulation
Interferons are signaling proteins
produced and released by host cells in
response to viral infection and other
immune stimuli.
Role in controlling viruses
Complement: A Versatile
Backup System
,
The complement system named for
its property of “
complementing ”
,
immune reactions consists of at least
30 blood proteins released by liver
, ,
cells lymphocytes and monocytes .
Three primary defensive
features of the complement
system
1. The membrane attack complex (MAC),
which kills pathogens directly
2. The coating of pathogens with molecules
that make them more attractive to
phagocytes (opsonization)
3. The recruitment of inflammatory cells and
triggering of cytokine release.
Third Line of Defense
Adaptive Immunity
Adaptive immunity provides long-lasting protection after exposure
to specific pathogens. Vaccination safely triggers this immune
response without causing disease. A key feature is the ability to
distinguish between the body's own cells ("self") and foreign
substances ("nonself"). Adaptive immunity activates when innate
defenses fail, tailoring responses to specific threats. It has a slower
primary response upon first exposure and a faster, stronger
secondary response due to immune memory.
Dual Nature of the Adaptive Immune System
Overview of Humoral Immunity
Humoral immunity refers to immune responses in body fluids, mediated
by antibodies (also called immunoglobulins) that target foreign molecules
called antigens. It mainly involves B lymphocytes (B cells), which, once
activated, produce specific antibodies against viruses, bacteria, and
toxins found outside cells. In humans, B cells are formed in the fetal liver
and later mature in the red bone marrow, eventually residing in the blood
and lymphoid organs.
Dual Nature of the Adaptive Immune System
Overview of Cellular Immunity
Cellular immunity, or cell-mediated immunity, is based on T
lymphocytes (T cells). Unlike B cells, T cells don’t directly bind to
antigens. Instead, phagocytic cells, like macrophages or dendritic
cells, process and present antigenic peptides to T cells. T cells have
receptors (TCRs) that recognize these peptides. Once activated,
some T cells destroy target cells presenting the antigen, while others
release cytokines to help other immune cells perform their functions.
T cells mature in the thymus and are found in the blood and lymphoid
organs. Cellular immunity is particularly effective against viruses and
certain intracellular bacteria, such as Listeria monocytogenes and
Mycobacterium leprae.
Cytokines: Chemical Messengers of Immune cells
,
Adaptive immunity involves complex interactions between immune cells mediated by chemical messengers called
cytokines. .
These are proteins or glycoproteins produced by immune cells in response to a stimulus There are over
200 , .
known cytokines each acting on cells with the corresponding receptors They are classified by structure or
, , , ,
function and include interleukins chemokines interferons tumor necrosis factors and hematopoietic cytokines , .
Interleukins (ILs) ,
communicate between leukocytes stimulating cell functions like proliferation and activation They .
can be used in treatments for infections and cancers .
Chemokines ,
guide leukocytes to infection sites to combat pathogens and are critical in conditions like HIV .
Interferons (IFNs) interfere with viral infections and are used as antiviral treatments for diseases like hepatitis and
cancer .
Tumor Necrosis Factor (TNF- α) plays a role in inflammation and autoimmune diseases, with therapies available to
block its effects .
Hematopoietic cytokines ,
control the development of blood cells with some used in therapies for bone marrow
transplants .
, .
Cytokines can also stimulate more cytokine production creating a feedback loop However if this process becomes ,
, ,
excessive it can result in a cytokine storm which can cause severe tissue damage and is involved in diseases like
,
influenza Ebola and sepsis , .
Cytokines: Chemical Messengers of Immune cells
Antigens and Antibodies
Antigens
Antigens are substances that induce the production of antibodies and are
usually proteins or large polysaccharides.
Pathogens can have multiple antigenic sites, such as components like capsules,
cell walls, flagella, fimbriae, bacterial toxins, and viral coats.
Nonmicrobial antigens include pollen, egg white, blood cell surface molecules,
and serum proteins from other individuals or species.
Detection of an antigen provokes the production of highly specific,
corresponding antibodies.
Antigens that cause an immune response are called immunogens.
Antigens and Antibodies
Antibodies react with specific regions on antigens
known as epitopes or antigenic determinants.
PAMPs (pathogen-associated molecular patterns)
are recognizable antigens on pathogens that
alert the host's immune system.
Haptens are low-molecular-mass substances
that are not antigenic unless combined with a
carrier molecule, such as penicillin, which can
trigger allergic reactions in some people.
Conjugated vaccines work by attaching an
antigen to a protein, similar to how haptens work.
Antigens and Antibodies
Humoral Immunity: Antibodies
Antibodies are soluble proteins that recognize and bind to specific antigens. They are secreted by plasma cells or attached to
B cells' membranes.
Each antibody has two identical antigen-binding sites and its valence refers to the number of these sites. Most human
antibodies are bivalent (two binding sites).
The antibody structure consists of four protein chains: two light chains and two heavy chains, forming a Y-shape. The ends of
the Y are variable regions (V regions), which bind to antigens, while the stem and lower arms are constant regions (C regions).
The stem is called the Fc region, which plays a key role in immune reactions, such as binding to complement proteins to destroy
pathogens.
Antigens and Antibodies
Immunoglobulin Classes:
IgG: The most abundant antibody in serum, protecting against bacteria, viruses, and toxins.
It crosses the placenta to provide passive immunity to the fetus.
IgM: The first antibody produced in response to a primary infection. It is large (pentamer)
and effective at causing clumping and complement activation.
IgA: Found in mucous membranes and body secretions like saliva, tears, and breast milk. It
prevents pathogens from attaching to surfaces in the respiratory and intestinal tracts.
IgD: Present in small amounts in serum and on B cells, aiding in immune responses.
IgE: Linked to allergic reactions and parasitic infections. It binds to mast cells and basophils,
triggering the release of histamine and other chemicals.
Each immunoglobulin class has distinct functions in protecting the body against infections and
other harmful agents.
Antigens and Antibodies
Humoral Immunity Response Process
Humoral immunity occurs in extracellular spaces and targets free antigens.
Antigen processing leads to the production of specific antibodies to
neutralize the antigen.
Memory B cells are created to ensure a faster immune response in future
encounters with the same antigen.
B cells carry immunoglobulins (mainly IgM and IgD) on their surface, each
specific for a particular epitope.
Some B cells, such as those in the intestinal mucosa, may carry other
immunoglobulins like IgA.
Humoral Immunity Response Process
Clonal expansion occurs when activated B cells produce plasma cells (which make antibodies) and memory
cells.
T-dependent antigens (mostly proteins from viruses, bacteria, red blood cells, or haptens) require help
from T helper (TH) cells to activate B cells.
o Both B and T cells must recognize different epitopes on the same antigen to ensure
specificity and prevent autoimmune responses.
T-independent antigens can directly activate B cells without the need for T cell assistance.
Humoral Immunity Response Process
-
Activation and Clonal Expansion of Antibody Producing Cells
Activation of Antigen-Presenting Cells (APCs): APCs (like B cells, macrophages, and dendritic
cells) bind to antigens, internalize them, and display digested fragments on their surface using
MHC (Major Histocompatibility Complex) molecules.
MHC Types:
o Class I MHC: Found on all nucleated cells, identifies cells as “self” to prevent immune
attacks on our own tissues.
o Class II MHC: Found on APCs, presents antigen fragments to attract T helper cells.
T Helper Cell Interaction: T helper cells bind to antigen fragments on the APC, release cytokines,
and activate B cells.
Humoral Immunity Response Process
:
Clonal Expansion Activated B cells undergo clonal
,
expansion producing plasma cells which make (
)
antibodies and memory cells which enhance (
future immune responses ).
- :
T Independent Antigens Directly stimulate B cells
,
without T cell help often consist of repeating
( . ., bacterial capsules).
subunits e g
o They induce a weaker immune response ,
,
mainly IgM and do not produce memory
cells.
'
o Infants immune systems may not respond
-
to T independent antigens until around age
2.
Humoral Immunity Response Process
The Diversity of Antibodies
(
Human immune system can produce a vast number of antibodies estimated
1:10¹⁵).
,
Small number of genes required for this diversity thanks to random
rearrangement of gene segments .
Gene rearrangements occur during B cell differentiation before antigen exposure .
( ) ,
Variable site V site on antibodies is created through this rearrangement leading
- .
to diverse antigen binding sites
Some B cell antigen receptors could produce antibodies that harm tissues but ,
these cells are usually eliminated through clonal deletion during immature
lymphocyte stage .
Results of the Antigen–Antibody Interaction
Antigen-Antibody Complex: When an antibody binds to its specific antigen,
they form an antigen-antibody complex.
Affinity: The strength of the bond between the antigen and antibody is
called affinity; higher affinity occurs when the antigen and antibody fit
closely.
Specificity: Antibodies recognize the amino acid sequence of the antigen's
epitope, giving specificity to the interaction. They can even distinguish minor
differences in amino acid sequences.
Diagnostic Use: Antibodies are used in diagnostics to differentiate between
viruses (e.g., hepatitis B vs. hepatitis C) and bacterial strains.
Antibody Functions: Antibodies do not destroy antigens directly but mark them
for destruction or neutralization by phagocytes and complement.
Results of the Antigen–Antibody Interaction
Mechanisms of Antibody Action:
o Agglutination: Antibodies cause antigens to clump together, aiding in
phagocytosis.
o Opsonization: Antibodies or complement proteins coat antigens, enhancing
phagocytosis.
o Antibody-Dependent Cell-Mediated Cytotoxicity: Antibodies coat the target,
but the phagocyte kills the target without engulfing it.
o Neutralization: IgG antibodies block microbes from attaching to host cells and
neutralize toxins.
o Complement Activation: IgG or IgM antibodies trigger the complement system,
causing microbial lysis and attracting immune cells.
Results of the Antigen–Antibody Interaction
Cellular Immunity Response Process
-
Humoral antibodies are effective against free floating pathogens ,
but not against intracellular antigens e g ( . ., viruses, bacteria,
parasites), which are inside host cells.
T cells evolved to combat intracellular pathogens and recognize
,
abnormal cells such as cancer cells .
T cells are specific to antigen fragments bound to MHC molecules .
About 98% of immature T cells are eliminated in the thymus through
thymic selection, ensuring only those that correctly recognize foreign
materials and host cells survive.
,
Once mature T cells migrate through the blood and lymphatic system
to lymphoid tissues to encounter antigens .
Cellular Immunity Response Process
Pathogens typically enter the body
through the gastrointestinal or
respiratory tracts, which are lined with
epithelial cells that have M cells.
M cells in the intestinal tract transport
antigens to lymphocytes and antigen-
presenting cells in Peyer’s patches, key
for the immune response.
Antibodies (primarily IgA) are produced
in the Peyer’s patches and migrate to
the mucosal lining, contributing to
mucosal immunity.
Cellular Immunity Response Process
-
Antigen Presenting Cells (APCs)
- ( )
Antigen Presenting Cells APCs involved in cellular
,
immunity include B cells dendritic cells and,
activated macrophages .
APCs have MHCs on their surfaces that present
,
antigenic fragments to T cells leading to T cell
activation .
APCs produce IL -12, which activates TH1 cells.
Cellular Immunity Response Process
Dendritic Cells:
Dendritic cells (DCs) have long dendrites and are
key APCs that induce immune responses in T cells.
Found in skin, genital tract, lymph nodes, spleen,
thymus, blood, but not the brain.
Act as sentinels, engulf invading microbes,
degrade them, and transfer them to lymph nodes
for display to T cells.
Cellular Immunity Response Process
Macrophages:
Macrophages are phagocytic cells involved in
innate immunity and removal of debris and
dead cells.
When activated, macrophages become
more motile and phagocytic, enhanced by
cytokines from T helper cells.
Activated macrophages play a role in
controlling cancer cells, virus-infected cells,
and intracellular pathogens (e.g., tubercle
bacillus).
After processing antigens, APCs migrate to
lymph nodes or mucosal lymphoid centers to
present the antigen to specific T cells.
Cellular Immunity Response Process
Classes of T Cells
: (
Classes of T Cells T cells are categorized by glycoproteins CD 4+ and CD8+) on their surfaces,
which determine their function .
(
T Helper Cells CD4+ T Cells): Recognize antigens presented by MHC class II molecules on APCs
and activate macrophages. They secrete cytokines, leading to the differentiation of TH1, TH2,
and TH17 subsets, each with distinct roles in immune responses, such as activating
macrophages or producing antibodies.
: , ,
T Regulatory Cells A subset of T helper cells they help control autoimmune reactions protect
,
microbiota and may play a role in pregnancy and establishing the skin microbiome .
·Cytotoxic T Lymphocytes (CD8+ T Cells): Initially, precursor CTLs (CTLp) become effector
CTLs that target and kill infected, tumor, or transplanted cells. They recognize antigens on the
surface of target cells presented by MHC class I molecules and induce cell death through
,
perforin and granzymes causing apoptosis .
Cellular Immunity Response Process
Nonspecific Cells and Extracellular Killing
by the Adaptive Immune System
Natural Killer (NK) Cells: NK cells are large granular leukocytes that can destroy virus-
infected cells, tumor cells, and parasites. Unlike CTLs, NK cells are not antigen-specific and
do not require prior stimulation by a specific antigen.
Target Recognition: NK cells detect abnormal cells by checking for MHC class I self-
antigens. Cells that lack these markers, such as virus-infected or tumor cells, are targeted
for destruction.
Mechanism of Action: NK cells induce cell death through the formation of pores in the
target cell's membrane, leading to lysis or apoptosis, similar to the action of CTLs.
Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC): NK cells, with the help of
antibodies from the humoral immune system, can target larger pathogens like fungi,
protozoa, and helminths by binding to the Fc regions of antibodies on the target cell,
leading to its destruction.
Nonspecific Cells and Extracellular Killing
by the Adaptive Immune System
Immunological Memory
( )
Secondary Memory Response Occurs after the primary :
,
response with a faster longer and stronger antibody , ,
production .
:
Memory Cells B cells become memory cells after initial
exposure and respond quickly to future encounters with the
same antigen .
:
Class Switching B cells switch from producing IgM to other
antibodies e g ( . ., , , )
IgG IgE IgA with the same antigenic
specificity .
:
Antibody Titer Reflects the amount of antibody in the
.
serum In the primary response there s a delay , ' (4-7 ),
days
,
with IgM first then IgG peaking at 10-17 .
days The secondary
response is faster and stronger .
- :
Long Term Immunity Memory cells remain for years or even
,
decades rapidly differentiating into plasma cells when re -
exposed to the antigen .
Types of Adaptive Immunity
Types of Immunity
Active Immunity: Developed when the immune system responds to microorganisms or foreign substances.
o Naturally acquired active immunity: Gained from exposure to antigens through illness and recovery.
Immunity may be lifelong (e.g., measles) or temporary (e.g., some intestinal diseases).
o Artificially acquired active immunity: Gained through vaccination, where antigens are introduced to
stimulate an immune response without causing infection.
Passive Immunity: Occurs when antibodies are transferred from one person to another.
o Naturally acquired passive immunity: Maternal antibodies are passed to the infant through the placenta
or breast milk, providing temporary immunity.
o Artificially acquired passive immunity: Involves injecting antibodies from a previously immune individual
into the body, offering immediate protection but for a limited time (e.g., postexposure prophylaxis for
diseases like rabies).
Types of Adaptive Immunity
The Immune System
The Immune System
It is the body’s defense team.
It protects you from germs like bacteria, viruses, and fungi that can make you
sick.
It works by finding and fighting anything that shouldn’t be in your body.
The immune system has different parts like white blood cells, antibodies, and
special organs (like the spleen and lymph nodes) that all work together.
When something harmful enters your body, your immune system attacks it to
keep you healthy.
ANTIGEN
An antigen is anything that causes your immune
system to react. It’s usually something foreign,
like a germ or a toxin.
Antigens include toxins, chemicals, bacteria, viruses,
or other substances that come from outside the
body. Body tissues and cells, including cancer cells,
also have antigens on them that can cause an
immune response.
ANTIBODY
An antibody is a special protein made by your
body to fight antigens. It sticks to the antigen to
help destroy it.
Antibodies help the body to fight microbes or the toxins (poisons)
they produce. They do this by recognising substances called
antigens on the surface of the microbe, or in the chemicals they
produce, which mark the microbe or toxin as being foreign. The
antibodies then mark these antigens for destruction.
IMMUNOGLOBULIN
Immunoglobulin is just another name for an
antibody. It’s the scientific word for these
protective proteins.
Intravenous immunoglobulin (IVIG) is a pooled antibody, and a
biological agent used to manage various immunodeficiency states
and a plethora of other conditions, including autoimmune,
infectious, and inflammatory states.
Active vs. Passive
Immunity
Feature Active Immunity Passive Immunity
Immunity acquired through the
Immunity developed by the body's own
Definition transfer of antibodies from another
immune response to an antigen.
source.
Source of Obtained from another individual
Antibodies
Produced by the individual's own B cells.
or animal.
Onset Takes time to develop (days to weeks). Provides immediate protection.
Short-term, lasting weeks to
Duration Long-lasting, potentially lifelong.
months.
Maternal antibodies, antibody
Examples Recovery from infections, vaccinations.
injections (e.g., antivenom).
Natural vs. Artificial
Immunity
Type Description Examples
Natural Recovering from diseases like
Active Immunity resulting from natural exposure to a pathogen. chickenpox or measles.
Immunity
Artificial Immunity acquired through medical interventions that Vaccinations for diseases like polio
Active introduce antigens. or influenza.
Immunity
Natural Immunity passed from mother to child through placenta or Maternal antibodies protecting
Passive breast milk. newborns.
Immunity
Artificial Immunity provided by the injection of antibodies from Administration of antivenoms or
Passive another source. immunoglobulin therapies.
Immunity
REFERENCES:
MICROBIOLOGY (2014) BY OLIVIA WILSON
MEDICAL MICROBIOLOGY (2016) BY DANI MARTINEZ
CELL BIOLOGY (2020) BY REESE MILLER
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