The document provides an overview of the immune system, detailing the mechanisms of both innate (nonspecific) and adaptive (specific) immunity, including cell types involved, their functions, and responses to pathogens. It covers components like phagocytic cells, natural killer cells, and antibody responses, as well as the inflammatory process and the role of antigens in triggering immune responses. Additionally, it discusses the diversity of antibodies and their classes, highlighting the importance of memory and specificity in the immune response.

1. IMMUNE SYSTEM
•Specific and nonspecific response
•Humoral immunity

2. IMMUNE SYSTEM
 Pathogen (disease-causing organism) can be
bacteria, fungus, virus, or multicellular parasite.
 Pathogen infects animal because the internal
environment of animal offer a suitable habitat.
 The animal body is the ideal habitat for the pathogen
to grow, reproduce, and medium for transportation
to the new environments.

3.  Thus, a defense system must be made up in order to
ward off the invasion of pathogen into the animal
body.
 Immune system recognizes the pathogen as foreign
body and respond by producing immune cells and
protein.

4. IMMUNITY
 Immunity is defined as an ability of the body to resist
invasion of pathogen or disease.
 A study of how the immune system of animal works is
called immunology.
 Immunity are divided into nonspecific immunity and
specific immunity.

5. Pathogens
(microorganisms
and viruses)
INNATE IMMUNITY Barrier defenses:
Recognition of traits Skin
shared by broad ranges Mucous membranes
of pathogens, using a Secretions
small set of receptors
Internal defenses:
Phagocytic cells
Rapid response Antimicrobial proteins
Inflammatory response
Natural killer cells
ACQUIRED IMMUNITY Humoral response:
Recognition of traits Antibodies defend against
specific to particular infection in body fluids.
pathogens, using a vast
array of receptors Cell-mediated response:
Cytotoxic lymphocytes defend
Slower response against infection in body cells.

6. NONSPECIFIC IMMUNITY
 Also known as innate immunity.
 Present before any exposure to pathogens.
 Act immediately upon infection.
 Divided into surface barrier and internal defenses.

7. SURFACE BARRIER
 Skin is an outer covering of an animal body which act
as primary defense system.
 Possess keratinized epithelial membrane that function
as a barrier and prevent the pathogen that swarm on
the skin.
 Keratin is resistant to most weak acids and bases
and to bacterial enzymes and toxins.

8.  Mucous membranes line all body cavities that open
to the exterior; the digestive, respiratory, urinary, and
reproductive tracts.
 Epithelial membranes produce a variety of protective
chemicals.

9.  The acidity of skin secretions (pH 3 to 5) inhibits
bacterial growth. Sebum contains chemical that are
toxic to bacteria.
 Vaginal secretion of adult females are very acidic.
 The stomach mucosa, secretes a concentrated
hydrochloric acid solution and protein-digesting
enzymes.

10.  Saliva, which cleanses the oral cavity and teeth.
 Lacrimal fluid of eye contains lysozyme, an enzyme
that destroys the bacteria.
 Sticky mucus traps many microorganisms that enter
the digestive and respiratory passageways.
 Tiny mucus-coated hairs inside the nose traps the
pathogen, preventing it from entering the lower
respiratory passages.

11. INTERNAL DEFENSES:CELLS AND
CHEMICALS
 Internal defenses involve phagocytic cells, natural
killer cells, antimicrobial proteins, and
inflammatory response.
 The inflammatory response enlists macrophages,
mast cells, all types of white blood cells, and other
chemicals that kill pathogen.
 The phagocytic cells are the cells that functions in
engulfing the pathogen.

12. PHAGOCYTIC CELLS
 If the pathogens succeed to get through the skin, then
the phagocytic cells will combat the pathogens.
 Phagocytic cells consist of monocytes,
macrophages, neutrophils and eosinophils.
 Pathogens are recognized by surface cell receptors
which are also known as TLR (Toll-like receptors).

13. EXTRACELLULAR Lipopolysaccharide
FLUID
Helper
TLR4 Flagellin
protein
WHITE
BLOOD
CELL
TLR5
VESICLE TLR9
TLR3 Inflammatory
responses
ds RNA

14.  Macrophages derived from white blood cells,
monocytes which leave and enter the tissues, and
develop into macrophages.
 Neutrophils, the most abundant type of white blood
cells.
 Eosinophils, white blood cells that weakly phagocyte
the pathogens.

15. HUMAN LYMPHATIC SYSTEM
Interstitial fluid
Adenoid
Tonsil
Lymph Blood
nodes capillary
Spleen Tissue Lymphatic
cells vessel
Peyer’s patches
(small intestine)
Appendix
Lymphatic
vessels
Lymph Masses of
node defensive cells

16. MECHANISM OF PHAGOCYTOSIS
 Phagocytic cell engulfs the particulate matter.
 Cytoplasmic extension of phagocyte cell bind to the
particulate matter and pull it into vacuole.
 Phagosome is formed.
 Phagosome fuses with lysosome, forming a
phagolysosome.

17. Microbes
PHAGOCYTIC CELL
Vacuole
Lysosome
containing
enzymes

18. NATURAL KILLER CELLS
 Function in lysing and killing the cancer cells and
virus-infected body cells.
 Natural killer cells act before the specific immune
system is activated.
 Able to detect and eliminate the virus infected cell and
cancerous cell (virus infected cell and cancerous cell
do not express class I MHC protein).

19.  The natural killer cells detect the cell which is lack of
self cell surface receptors (class I MHC protein).
 Natural killer cells also promote the target cells to
undergo apoptosis (programmed cell death).

20. INFLAMMATORY RESPONSE
 The benefits of inflammatory response:
1. Prevent the spread of damaging agents to nearby
tissues.
2. Disposes of cell debris and pathogen.
3. Set the stage for repair (blood clotting).

21. INFLAMMATORY RESPONSE
 Factors which elicit inflammatory response:
1. Physical trauma ( a blow)
2. Intense heat
3. Irritating chemicals
4. Infection by viruses, fungi, and bacteria
The four cardinal signs of accute inflammation:
1. Pain
2. Redness
3. Heat
4. Swelling

22. Tissue
injured
Histamine (released by
basophils),chemical
mediators, prostaglandin,
complement kinin
Vasodilation of Increased Attract neutrophils,
arterioles capillary monocytes, and
•Local hyperemia permeability lymphocytes to
(increased blood flow •Capillaries leak injured area
to injured area fluid (exudate) (chemotaxis)
•Pus formation

23.  Mast cells- key components of inflammatory
response., release histamine.
 Pus- break down tissue, die or dying neutrophils,
dead or living pathogen, accumulate in the wound.
 Hyperemia (congestion of blood)- causes redness
and heat of an inflammed region.

24.  Inflammation can be divided into local inflammation
and systemic inflammation.
 Fever is an example of systemic inflammation. It is
triggered by pyrogens. The high body temperature
inhibits the microbial multiplication and enhances
body repair.

25.  Exudates- fluid containing antibodies and clotting
factors.
 Secretion of exudate causes local edema (swelling)
and contributes to the sensation of pain.

26. Splinter
Chemical Macrophage Fluid
Mast cell signals
Capillary Phagocytosis
Red blood cells Phagocytic cell
Major events in a local inflammatory responses

27. INFLAMMATORY CHEMICALS
CHEMICAL SOURCE PHYSIOLOGICAL
EFFECTS
Histamine Granules of basophils and mast cells, released Promotes vasodilation of local
in response to mechanical injury, presence of arterioles, increases permeability of
certain microorganisms, and chemicals local capillaries, promoting exudate
released by neutrophils. formation.
Kinins A plasma protein, kininogen is cleaved by the Same as for histamine, also induce
enzyme kallikrein found in plasma, urine, chemotaxis of leukocytes and
saliva, and lysosomes of neutrophils, and other prompt neutrophils to release
types of cells, cleavage releases active kinin lysosomal enzymes, thereby
peptides. enhancing generation of of more
kinin, induce pain.
Prostaglandins Fatty acid molecules produced from Sensitize blood vessels to effects
arachidonic acid-found in all cell membranes; of other inflammatory mediators,
generated by enzymes of neutrophils, one of the intermediate steps of
basophils, mast cells and others. prostaglandin generation produces
free radicals, which can cause
inflammation; induce pain.

28. ADAPTIVE/ SPECIFIC IMMUNITY
 Specific; recognizes and respond to specific pathogens
or foreign substances.
 Systemic; Immunity not only involve to the initial
infection site.
 Possess ‘memory’; Able to mount stronger attacks on
the pathogens which encounter the body previously.

29.  Adaptive immunity are divided into humoral
response and cell-mediated response.
 Humoral response involves the production of
antibody.
 Cell-mediated immunity involves cytotoxic cells.

30. HUMORAL RESPONSE
 Antibody-mediated immunity.
 Production of antibodies by lymphocytes.
 Antibodies present in the body’s “humors,” or fluids
(blood, lymph).
 Involve antigen recognition, antigen presenting, and B
cell proliferation.

31. B cells undergo maturity (antigen
binds to its surface receptor, Tcells
nearby)
B cells undergo clonal
selection (reproduce
asexually by mitosis)
Plasma cells
Antibodies Long-lived memory
cells

32. Humoral (antibody-mediated) immune response
Antigen (1st exposure)
Stimulates Engulfed by
Gives rise to
Antigen-
presenting cell
B cell Helper T cell
Memory
Helper T cells
Antigen (2nd exposure)
Plasma cells Memory
B cells
Secreted
antibodies
Defend against extracellular pathogens

33. Antigen-
presenting
cell Peptide antigen
Bacterium
Class II MHC molecule
CD4
TCR (T cell receptor)
Humoral Cytokines Helper T cell
immunity
Cell-mediated
(secretion of
immunity
antibodies by
(attack on
plasma cells
infected cells)
B cell Cytotoxic T cell

34. LYMPHOCYTES
(B CELLS AND T CELLS)
 B cells and T cells are lymphocytes.
 Involve in the humoral immune response.
 B cells are originated from the bone marrow.
 T cells are also originated from the bone marrow but it
migrated to the thymus.

35. ANTIGEN
 Antigens are foreign substances which elicits adaptive
immune response.
 Antigens are either natural or synthetic.
 Nonself; antigens are normally not parts of the body.
 Most antigens are large and complex molecules.

36.  To elicit adaptive immunity, antigen recognition must
occur.
 Antigen recognition- the B cell and T cell bind to the
antigen.
 The antigen binding- via antigen receptor which
attached to the surface of B cell and T cell plasma
membranes.

37. B CELL RECEPTOR
Antigen-
Antigen- binding site
binding Disulfide
site bridge
V
V Variable
regions
Light C C Constant
chain regions
Transmembrane
region
Plasma
Heavy chains membrane
B cell
(a) B cell receptor

38. T CELL RECEPTOR
Antigen-
binding
site
Variable
regions V V
Constant
regions C C
Transmembrane
region
Plasma
membrane
Disulfide bridge
Cytoplasm of T cell T cell
(b) T cell receptor

39. B CELLS ANTIGEN RECEPTORS
Y-shaped.
Consist four polypeptide chains. Two identical light chains
and two identical heavy chains.
Have constant region (C) and variable region (V).
When the antigen receptors bind to an antigen, B cell
activation occurs.

40.  The antigen receptor bind to the epitope.
 Epitope- Also known as antigenic determinant, a
small, accesible portion of an antigen that binds to an
antigen receptor.

41.  An antigen possesses several different epitopes.
 All the antigen receptors which are located at a single
lymphocyte only bind to the same epitope.
 When the antigen bind to the antigen receptor, B cell
activates and give rise to plasma cells.
 Plasma cells produce antibodies.

42. Epitopes
(antigenic
determinants)
Antigen-binding sites
Antigen
Antibody A
Antibody C
C C
C C Antibody B

43. ANTIBODIES
 Also known as immunoglobulins.
 Similar structure with B cell antigen receptors, but
antibodies do not attach to the surface cell
membranes.

44. ANTIBODY CLASSES
 Antibodies are divided into five major classes.
 Polyclonal antibodies- products of many different
clones of B cells following exposure to a microbial
agent.
 Monoclonal antibodies- prepared a single clone of B
cells grown in culture.

45. Class of Immuno- Distribution Function
globulin (Antibody
IgM First Ig class Promotes neutraliza-
(pentamer) produced after tion and cross-
initial exposure to linking of antigens;
antigen; then its very effective in
concentration in complement system
the blood activation
declines
IgG Promotes
(monomer) Most abundant Ig opsoniz
class in blood; a-
also present in tion,
tissue fluids neutraliz
ation,
and cross-linking
of
crosses placenta,
antigens; less
thus conferring
effec-
passive immunity
on fetusactivation
tive in
of
IgA Present in Provides localized
complement
(dimer) secretions such defense of mucous
system
as tears, saliva, membranes by
than IgM
mucus, and cross-linking and
breast milk neutralization of
antigens
Triggers release from
IgE Present in blood mast cells and
(monomer) at low concen- basophils of hista-
trations mine and other
chemicals that cause
allergic reactions
IgD
(monomer) Present Acts as antigen
primari receptor in the
ly antigen-
on surface of stimulat
B cells that have ed
not been proliferation and
expos differentiation of
ed B cells (clonal
to antigens selection

46. Class of Immuno-
Distribution Function
globulin (Antibody)
IgM First Ig class Promotes neutraliza-
(pentamer) produced after tion and cross-
initial exposure to linking of antigens;
antigen; then its very effective in
concentration in complement system
the blood declines activation
J chain

47. Class of Immuno-
Distribution Function
globulin (Antibody)
IgG
(monomer) Most abundant Ig Promotes opsoniza-
class in blood; tion, neutralization,
also present in and cross-linking of
tissue fluids antigens; less effec-
tive in activation of
complement system
than IgM
Only Ig class that
crosses placenta,
thus conferring
passive immunity
on fetus

48. Class of Immuno-
Distribution Function
globulin (Antibody)
IgA
(dimer) Present in Provides localized
secretions such defense of mucous
as tears, saliva, membranes by
mucus, and cross-linking and
J chain breast milk neutralization of
antigens
Presence in breast
milk confers
Secretory passive immunity
component on nursing infant

49. Class of Immuno-
globulin (Antibody) Distribution Function
IgE
Present in blood Triggers release from
(monomer)
at low concen- mast cells and
trations basophils of hista-
mine and other
chemicals that cause
allergic reactions

50. Class of Immuno-
Distribution Function
globulin (Antibody)
IgD Present primarily Acts as antigen
(monomer) on surface of receptor in the
B cells that have antigen-stimulated
not been exposed proliferation and
to antigens differentiation of
B cells (clonal
selection)
Trans-
membrane
region

51. ANTIBODY TARGETS AND
FUNCTIONS
 Neutralization- antibodies block specific sites on
viruses or bacterial exotoxins (toxin chemicals
secreted by bacteria).
 The virus or exotoxin cannot bind to the receptors on
tissue cells to cause injury.

52.  Agglutination- Antibodies bind to the antigenic
determinant on more on one antigen at a time.
 Forming antigen-antibody complexes which causes
clumping of the foreign cells.

53.  Precipitation- Soluble molucles are cross-linked into
large complexes that settle out of solution.

54.  Complement fixation and activation- Antibodies bind
to cells, cause the antibodies to change its shapes.
 The antibodies expose the transmembrane regions.
 Complement fixation into the antigenic cell’s surface
is triggered, followed by the cell lysis.

55. Viral neutralization Opsonization Activation of complement system and pore formation
Bacterium
Complement proteins
Virus
Formation of
membrane
attack complex
Macrophage
Flow of water
and ions
Pore
Foreign
cell

56. ANTIGEN RECOGNITION
 B cell antigen receptors – bind to the epitopes of
antigens.
 T cell antigen receptor – bind to the fragments of
antigens that are presented on the surface of host
cells.

57. MHC
 Major Histocompatibility Complex molecule.
 Encodes a group of glycoproteins called MHC
proteins.
 MHC proteins are divided into two groups, Class I
MHC proteins and Class II MHC proteins.

58. Class I MHC protein Class II MHC protein
Found on virtually all body cells. Found only on certain cells that acts
on immune system.
Involves in the cell-mediated Involves in the humoral immunity.
immunity.

59. RECOGNITION OF PROTEIN
ANTIGENS BY T CELLS
 The antigen is engulf by the cell. The antigen is
cleaved by host cell’s enzyme into antigen fragment.
 Antigen fragment binds to MHC molecule.
 Antigen fragment-MHC complex is brought to the
surface of the cell.
 T cell recognizes the antigen fragment-MHC complex.

60. THE ROLE OF THE MHC
 Bind to antigen fragment.
 Transport the antigen fragment to the surface of the
cell.
 Lead to antigen presentation, the display of the
antigen fragment on the cell surface.

61. HELPER T CELLS
 Activates the adaptive immune response.
 Antigen fragment is presented by class MHC proteins
on the host cell.
 The host cell which displays the antigen fragment is
called antigen-presenting cell.

62.  In the cell mediated immunity, the Class I MHC
protein formed a complex with the antigen fragment.
 In the humoral immunity, the antigen fragment forms a
complex with the Class II MHC protein.

63. Top view: binding surface
exposed to antigen receptors
Antigen
Class I MHC Antigen
molecule
Plasma
membrane of
infected cell

64. Antigen-
Infected cell Microbe presenting
1. cell
Antigen Antigen
fragment associat
es with Antigen
MHC fragment
Class I MHC molecul
molecule e
Class II
T cell MHC
receptor molecule
2. Tcell
T cell
recognize receptor
s
combinati
a) Cytotoxic T cell
on
b) Helper T cell

65. B CELL AND T CELL DEVELOPMENT
 The antigen presenting leads to B cell and T cell
activation.
 B cell is activated (stimulated to undergo
differentiation).
 B cell proliferates to form clones.
 The clones bear the same antigen-specific
receptors, similar to the activated B lymphocyte cell.

66.  Some cells from the clones form effector cells.The
effector cells which form from the B cells are plasma
cells.

67.  T cell is activated and proliferates to form clones.
Some of the clones become effector cells.
 The effector cells which arise from T cells are divided
into helper T cells and cytotoxic T cells.

68. CLONAL SELECTION
 The proliferation of B cells is the example of clonal
selection process.
 B cells form clones, a group of cell which are identical
to the original cell.

69. MONOCLONAL ANTIBODY
 Providing passive immunity.
 Are made by fusing tumor cells and B lymphocytes.
 The resulting cell are called hybridomas.
 Hybridomas proliferates in culture, and produce a
single type of antibody.
 Used to diagnose pregnancy, sexually transmitted
diseases, hepatitis and rabies.

70. CELL MEDIATED IMMUNITY
 Involve the cytotoxic T cells.
 Cytotoxic cells- destroy any cells in the body that
harbor anything foreign.

71. Released cytotoxic T cell
Cytotoxic T cell
Perforin
CD8 Dying target cell
Class I Granzymes
MHC Pore
molecule TCR
Targe
t
cell
The killing action
of cytotoxic T cells

72. CYTOTOXIC T CELL
 T cells which undergo proliferation will form effector
cells.
 The effector cells are helper T cells and cytotoxic T
cells.
 The surface of the cytotoxic T cells have glycoproteins
called CD8 (different from the helper T cells which
possess CD4).
 All body cells display class I MHC antigens, so all
infected cells or abnormal cells can be destroyed by
cytotoxic T cells.

73. Humoral (antibody-mediated) immune response Cell-mediated immune response
Antigen (1st exposure)
Stimulates
Engulfed by Gives rise to
Antigen-
presenting cell
B cell Helper T cell Cytotoxic T cell
Overview
Memory
Helper T cells of
acquired/
adaptive
Antigen (2nd exposure)
Plasma cells Memory B cells Memory Active immune
Cytotoxic T cells
Cytotoxic T
cells
system
Secreted
antibodies
Defend against extracellular pathogens by binding to antigens, Defend against intracellular pathogens
thereby neutralizing pathogens or making them better targets and cancer by binding to and lysing the
for phagocytes and complement proteins . infected cells or cancer cells .