The adaptive immune system has four defining characteristics: self/non-self recognition, specificity, diversity, and memory. B and T lymphocytes recognize antigens through surface receptors and respond by dividing into effector cells that combat infection, and memory cells that remember each antigen. The antibody-mediated response involves B cells producing antibodies against extracellular pathogens, while the cell-mediated response uses cytotoxic T cells and natural killer cells to destroy infected or abnormal body cells.

1. Immunity

2. 38.1 Integrated Responses to Threats
 Immunity
• The capacity to resist and combat infection by
pathogens such as viruses, bacteria, and fungi
 In vertebrates, innate and adaptive immune
systems work together to combat infection and
injury

3. Evolution of the Body’s Defenses
 Proteins in eukaryotic cell membranes have
unique patterns that the body recognizes as self
 Cells of multicelled eukaryotes have receptors
that recognize nonself cues (PAMPs) on or in
pathogens, and trigger defense responses

4. Innate Immunity
 Binding of a receptor with a PAMP triggers
immediate, general defense responses that are
part of inborn innate immunity
 Complement
• Proteins that destroy microorganisms or flag them
for phagocytosis
• An innate immune response

5. Adaptive Immunity
 Adaptive immunity is a system of defenses that
specifically targets billions of different antigens
an individual may encounter during its lifetime
 Antigen
• PAMP or other molecule the body recognizes as
nonself that triggers an active immune response

6. Three Lines of Defense
1. Physical, chemical, and mechanical barriers
• Keep pathogens outside the body
2. Innate immunity
• General responses destroy invaders inside the
body before they become established
3. Adaptive immunity
• Huge populations of white blood cells form to
target and remember a specific antigen

7. Mucus and Cilia: Physical Barriers

8. Comparing Innate and Active Immunity

9. The Defenders
 White blood cells (leukocytes) specialized for
different tasks carry out all immune responses
• Phagocytes (neutrophils, macrophages,
dendritic cells)
• Secretory cells (eosinophils, basophils, mast
cells
• Lymphocytes (B and T lymphocytes, natural
killer cells)

10. The Defenders
 All white blood cells secrete chemicals, including
cell-to-cell signaling molecules (cytokines) that
coordinate all aspects of immunity
• Interleukins
• Interferons
• Tumor necrosis factors

11. White Blood Cells

12. Fig. 38-3a, p. 661

13. Fig. 38-3b, p. 661

14. Chemical Weapons of Immunity

15. 38.1 Key Concepts
Overview of Body Defenses
 The vertebrate body has three lines of immune
defenses
• Surface barriers prevent invasion by ever-present
pathogens
• General innate responses rid the body of most
pathogens
• Adaptive responses specifically target pathogens
and cancer cells

16. 38.2 Surface Barriers
 Normal flora
• Billions of microorganisms normally live on
human surfaces, including interior tubes and
cavities of digestive and respiratory tracts
 A pathogen can cause infection only if it enters
the internal environment by penetrating skin or
other protective barriers at the body’s surfaces

17. Some Normal Flora

18. Vertebrate Surface Barriers
 Physical, chemical, and mechanical barriers
keep microorganisms outside body tissues
• Skin
• Mucus and cilia
• Lysozyme
• Gastric fluid and bile salts
• Normal flora
• Urination

19. Vertebrate Surface Barriers

20. Skin
 Healthy, intact skin is an effective surface barrier

21. Fig. 38-5, p. 663
skin surface
epithelial
cells die and
become filled
with keratin
as they are
pushed toward
skin surface
epidermis
dividing
epithelial
cells
0.1 mm

22. 38.3 Remember to Floss
 Dental plaque
• A thick, sticky biofilm of glycoproteins, bacteria,
and their products that contribute to tooth decay
and gum disease (periodontitis)
 Nine of every ten cardiovascular disease
patients have serious periodontal disease
 Oral bacteria associated with periodontitis are
also found in atherosclerotic plaque

23. Plaque

24. 38.2-38.3 Key Concepts
Surface Barriers
 Skin, mucous membranes, and secretions at the
body’s surfaces function as barriers that exclude
most microbes

25. 38.4 Innate Immune Responses
 Innate immune mechanisms nonspecifically
eliminate pathogens that invade internal tissues
before they become established
• Phagocytes
• Complement
• Inflammation
• Fever

26. Phagocytes
 Macrophages
• Large phagocytes that patrol interstitial fluid and
engulf and digest pathogens
• Secrete cytokines when receptors bind to antigen
• Cytokines attract more macrophages, neutrophils,
and dendritic cells to infection site

27. Complement
 Complement proteins become activated when
they encounter antigen
• Cascading enzyme reactions concentrate
activated complement at infection site
• Complement attracts phagocytes to infection site
and tags pathogens for destruction
• Forms attack complexes that puncture bacteria
• Helps mediate active immunity

28. Complement Attack Complexes

29. Fig. 38-7a, p. 664
A In some responses, complement proteins become activated when
antibodies (the Y-shaped molecules) bind to antigen—in this case, antigen
on the surface of a bacterium.
activated
complement
antibody
molecule

30. Fig. 38-7b, p. 664
B Complement also becomes activated when it binds directly to antigen.
activated
complement
bacterial cell

31. Fig. 38-7c, p. 664
C By cascading
reactions, huge numbers
of different complement
molecules form and
assemble into structures
called attack complexes.
activated
complement

32. Fig. 38-7de, p. 664
D The attack complexes
become inserted into the
target cell’s lipid envelope or
plasma membrane. Each
complex makes a large pore
form across it.
attack complex
that causes a
pore to form
through the lipid
bilayer of the
bacterium
E The pores bring
about lysis of the cell,
which dies because
of the severe
structural disruption.

33. Inflammation
 Inflammation
• A local response to tissue damage characterized
by redness, warmth, swelling and pain, triggered
by activated complement and cytokines
• Mast cells release histamine, increasing capillary
permeability
• Phagocytes and plasma proteins leak out, attack
invaders, form clots, and clean up debris

34. Inflammation Response
to Bacterial Infection

35. Fig. 38-8, p. 665
A Bacteria
invade a tissue
and release
toxins or
metabolic
products that
damage tissue.
B Mast cells in
tissue release
histamine, which
widens arterioles
(causing redness
and warmth) and
increases
capillary
permeability.
C Fluid and
plasma
proteins leak
out of
capillaries;
localized
edema (tissue
swelling) and
pain result.
D Complement
proteins attack
bacteria.
Clotting factors
also wall off
inflamed area.
E Neutrophils and
macrophages engulf
invaders and debris.
Macrophage
secretions kill
bacteria, attract
more lymphocytes,
and initiate fever.
Stepped Art

36. Fever
 Fever
• A temporary rise in body temperature – above the
normal 37°C (98.6°F) – that often occurs in
response to infection
• Cytokines stimulate brain cells to release
prostaglandins, which act on the hypothalamus
• Fever enhances the immune response by
speeding up metabolism and phagocyte activity
• Fever over 40.6°C (105°F) can be dangerous

37. 38.4 Key Concepts
Innate Immunity
 Innate immune responses involve a set of
general, immediate defenses against invading
pathogens
 Innate immunity includes phagocytic white blood
cells, plasma proteins, inflammation, and fever

38. Evolution of the Body’s Defenses
 Proteins in eukaryotic cell membranes have
unique patterns that the body recognizes as self
 Cells of multicelled eukaryotes have receptors
that recognize nonself cues (PAMPs) on or in
pathogens, and trigger defense responses

39. 38.5 Overview of Adaptive Immunity
 Vertebrate adaptive immunity adapts to different
antigens it encounters during its lifetime
 Lymphocytes and phagocytes interact to effect
four defining characteristics: Self/nonself
recognition, specificity, diversity, and memory

40. Self/Nonself Recognition
 Self versus nonself recognition
• Each kind of cell or virus has a unique identity
 MHC markers
• Plasma membrane self-recognition proteins
 T cell receptors (TCRs)
• Antigen receptors that recognize MHC markers
as self, antigens as nonself

41. Specificity and Diversity
 Specificity
• Defenses are tailored to target specific antigens
 Diversity
• There are potentially billions of different antigen
receptors on T and B cells

42. Memory
 Memory
• The capacity of the adaptive immune system to
remember an antigen
• If the same antigen appears again, B and T cells
make a faster, stronger response

43. HOW IT WORKS?

44. First Step – The Antigen Alert
 Once a B or T cell recognizes and binds to a
specific antigen, it begins to divide by mitosis
• All descendent cells recognize the same antigen
 T cells do not recognize an antigen unless it is
presented by an antigen-presenting cell
• Macrophages, B cells, and dendritic cells digest
particles and display antigen-MHC complexes

45. Cell Types
 Effector cells
• Differentiated lymphocytes (B and T cells) that act
at once to fight infection
 Memory cells
• Long-lived B and T cells reserved for future
encounters with the same antigen

46. Antigen Processing

47. Fig. 38-9a, p. 666

48. cell engulfs
an antigen-
bearing
particle
Fig. 38-9b, p. 666
antigen–MHC complexes
become displayed on
cell surface
endocytic
vesicle forms
MHC markers
bind fragments
of particle
particle is
digested
into bits
lysosome
fuses with
endocytic
vesicle
Stepped Art

49. Two Arms of Adaptive Immunity
 Antibody-mediated immune response
• B cells produce antibodies that bind to specific
antigen particles in blood or interstitial fluid
 Cell-mediated immune response
• Cytotoxic T cells and NK cells detect and destroy
infected or altered body cells

50. Interactions Between Antibody-Mediated
and Cell-Mediated Responses

51. Intercepting and Clearing Out Antigen
 After engulfing antigen-bearing particles,
dendritic cells or macrophages migrate to lymph
nodes, where T cells bind and initiate responses
 During an infection, lymph nodes swell due to
accumulation of T cells
 Antibody-antigen complexes bound by
complement are cleared by the liver and spleen

52. The Lymphatic System

53. Fig. 38-11, p. 667
lymph node,
midsection
(thymus
gland)
spleen

54. 38.6 Antibodies
and Other Antigen Receptors
 Antigen receptors on B and T cells have the
potential to recognize billions of different antigens
 Antibody
• Y-shaped antigen receptor (protein), made only by
B cells, that binds only to the antigen that
prompted its synthesis
• Activates complement, facilitates phagocytosis, or
neutralizes pathogens or toxins

55. Fig. 38-12b, p. 668
binding site for antigen
variable region
(dark green) of
heavy chain
binding site for antigen
variable region
of light chain
constant region
of light chain
constant region (bright
green) of heavy chain,
including a hinged region

56. Five Classes of Antibodies
 Constant regions determine 5 classes of
antibodies (immunoglobins IgG, IgA, IgE, IgM,
and IgD), each with different functions
 B cell receptors are membrane-bound IgM or
IgD antibodies

57. Making Antigen Receptors
 Genes that encode antigen receptors occur in
several segments on different chromosomes
 Different versions are randomly spliced together
during B or T cell differentiation, producing about
2.5 billion different combinations
 T cells mature in the thymus, which stimulates
production of MHC and T cell receptors

58. Antigen Receptor Diversity

59. 38.7 The Antibody-Mediated
Immune Response
 Antibody-mediated immune response
• Antigen activates naïve B cells and dendritic cells
• Naïve T cell binds to APC and differentiates into
effector and memory helper T cells
• Helper T cells bind antigen-MHC complexes on
activated B cell and secrete cytokines
• B cell differentiates into effector B cells, which
produce antibodies targeting a specific antigen,
and memory B cells

60. Fig. 38-14, p. 670
Stepped Art
A
naive
B cell
B cell
complement
A The B cell receptors on a naïve
B cell bind to a specific antigen on
the surface of a bacterium
dendritic
cell
B
bacterium
antigen-
presenting
dendritic
cell
B The dendritic cell engulfs the
same kind of bacterium that the B
cell encountered.
D cytokines
D Antigen receptors of one of the
effector helper T cells bind
antigen-MHC complexes on the B
cell.
E
memory
B cell
effector
B cell
E The cytokines induce the B cell
to divide, giving rise to many
identical B cells.
F
F The effector B cells begin
making and secreting huge
numbers of IgA, IgG, or IgE.
C The antigen-MHC complexes on
the antigen-presenting cell are
recognized by antigen receptors on
a naïve T cell.
naive
T cell
effector
helper T
cell
memory
helper T
cell
C

61. Clonal Selection and Memory Cells
 Only B cells with receptors that bind antigen
divide (clone) and differentiate into effector and
memory B cells
 First exposure (primary response) produces
memory B and T cells; secondary response is
stronger and faster

62. Fig. 38-15a, p. 671
antigen
Antigen binds only
to a matching B cell
receptor.
mitosis
clonal
population
of effector
B cells
Many effector B cells secrete many antibodies.

63. Fig. 38-15b, p. 671
B cell with bound antigen
mitosis
primary
immune
response
effector cells memory cells
mitosis
secondary
immune
response
effector cells memory cells

64. Primary and Secondary
Immune Response

65. 38.8 The Cell-Mediated Response
 Cell-mediated immune response
• Dendritic cell ingests altered body cell, displays
antigen-MHC complexes, migrates to lymph node
• Naïve helper T and cytotoxic T cells bind to APC
• Activated helper T divides and differentiates into
memory and effector cells; cytokines signal
division of activated cytotoxic T cells
• Cytotoxic T cells circulate and touch-kill altered
body cells

66. Fig. 38-17, p. 672
Stepped Art
dendritic
cell
A
antigen-
presenting
dendritic
cell
A A dendritic cell engulfs a
virus-infected cell.
naive
cytotoxic
T cell
C
activated
cytotoxic
T cell
C Receptors on a naïve cytotoxic
T cell bind to the antigen-MHC
complexes on the surface of the
dendritic cell.
D
cytokines
memory
cytotoxic T
cell
effector
cytotoxic
T cell
D The activated cytotoxic T cell
recognizes cytokines secreted by
the effector helper T cells as
signals to divide.
E E The new cytotoxic T cells
circulate through the body.
B
effector
helper T
cell
memory
helper T
cell
B Receptors on a naïve helper T
cell bind to antigen-MHC
complexes on the dendritic cell.
naive
helper T
cell

67. Cytotoxic T Cells
 Cytotoxic T cells touch-kill cells displaying
antigen-MHC markers; perforin and proteases
puncture cells and kill them by apoptosis

68. Fig. 38-18b, p. 673
cytotoxic
T cell
cancer
cell

69. Natural Killer Cells
 Cytokines secreted by helper T cells also
stimulate natural killer (NK) cell division
 Unlike cytotoxic T cells, NK cells can kill infected
cells that are missing all or part of their MHC
markers

70. 38.5-38.8 Key Concepts
Adaptive Immunity
 In an adaptive immune response, white blood
cells destroy specific pathogens or altered cells
 Some make antibodies in an antibody-mediated
immune response; others destroy ailing body
cells in a cell-mediated response

71. 38.10 Vaccines
 Immunization
• The administration of an antigen-bearing vaccine
designed to elicit immunity to a specific disease
 Vaccine (active immunization)
• A preparation containing an antigen that elicits a
primary immune response
 Passive immunization
• Administration of antibodies; no immune response

72. Smallpox Vaccine
 Edward Jenner created the first vaccine against
smallpox, which has now been eradicated

73. Recommended Immunizations

74. Autoimmune Disorders
 Sometimes lymphocytes and antibodies fail to
discriminate between self and nonself
 Autoimmune response
• An immune response that is misdirected against
the person’s own tissues
• Rheumatoid arthritis, Graves’ disease, multiple
sclerosis

75. Immunodeficiency
 In immunodeficiency, the immune response is
insufficient to protect a person from disease
 Primary immune deficiencies are present at birth
• SCIDs, ADA
 Secondary immune deficiency results from
exposure to an outside agent, such as a virus
• AIDS