class on humoral immunity

1. Dr Ashwani kumar
CELLULAR AND HUMORAL
IMMUNITY AND STRUCTURE
OF ANTIBODIES

2. I. Definition of antigens
Antigens are the substance which when introduced parenterally into
the body stimulates the production of an antibody with which it
reacts specifically and in an observable manner.
Specificity is referred to that, immune responses are directed toward and able to
distinguish between distinct antigen or small parts of macromolecular antigens.
Ab1 Ab2 Ab3

3. How Antigen enters
Sites of antigen entry
Sites of
initial antigen capture
Sites of antigen
collection and capture

4. 1.
Immunogen:
the antigen
that induce
specific
immune
response
2.Tolerogen:
antigen that
induce
Immunologic
tolerance
Immunologic
tolerance is
unresponsiveness
to an antigen that
is induced by prior
exposure to that
antigen.
3.Allergen: antigen
that induce
Anaphylaxis (severe
immediate
hypersensitivity
reaction occurring as
a result of rapid
generalized mast-cell
granulation)
4. Vaccine:
antigens that
induce a
protection
immune
response
against
microbes and
are used to
prevent
diseases

5. Superantigens
Superantigens are the third variety of biological class of
antigens, recently described in the last decade.
Unique feature of superantigens is, they can activate T cells
directly without being processed by antigen presenting
cells (APCs).
The variable β region of T cell receptor (vβ of TCR) appears
to be the receptor for superantigens.

6. Superantigen
Bacterial superantigen
Staphylococcal toxin-
 Toxic shock syndrome toxin-1(TSST-1); Exfoliative
toxin;Enterotoxins
Streptococcal toxin- Streptococcal pyrogenic exotoxin (SPE)-
A and C
Mycoplasma arthritidis mitogen-I
Yersinia enterocolitica
Yersinia pseudotuberculosis
Viral superantigen
Epstein-Barr virus associated superantigen
Cytomegalovirus associated superantigen
Rabies nucleocapsid
HIV encoded superantigen (nef- negative regulatory factor)
Fungal superantigen
Malassezia furfur

7. Immunogenecity vs
Antigenicity
 Immunogenicity is the ability to induce a humoral
and/or cell-mediated immune response.
B cells + antigen
T cells + antigen
effector B cells + memory B cells
effector T cells + memory T cells
Antigenicity is the ability to combine specifically with the
final products of the immune response (i.e. secreted
antibodies and/or surface receptors on T- cells).
Although all molecules that have the property of
immunogenicity also have the property of antigenicity, the

8. Classification of Antigens
Complete antigen
Which contains both
immunogenicity and
antigenicity
Incomplete antigen
Contains only antigenicity
e.g. Haptens
Proteins
Majority of immunogens are proteins
(pure proteins or they may be
glycoproteins or lipoproteins). Proteins
are usually very goodimmunogens.
Polysaccharides
Pure polysaccharides and
lipopolysaccharides are good
immunogens.
Nucleic Acids
Nucleic acids are usually poorly
immunogenic. However, they may
become immunogenic when single
stranded or when complexed with
proteins.
Lipids
In general lipids are non-immunogenic,
although they may be haptens.
TD-Ag (thymus
dependent antigens
)
TI-Ag (thymus
independent
antigens)

9. 1.Antigen determinants (epitope)
The portion of antigen molecules which can be specifically
recognized by antibody or antigenic receptor of lymphocytes.

10. Classification of antigenic determinant
1.According to the structure of Antigen determinants
Conformational
determinants : are
formed by amino acid
residues that aren’t in a
sequence but become
spatially juxtaposed in
the folded protein
Sequential (or linear)
determinants
Epitopes formed
by several adjacent
amino acid residues
are called linear
determinants.

11. 2.According to types of cells recognizing antigenic determinants
T cell epitope B cell epitope
Receptor TCR BCR
Nature short peptide proteins, polysaccharides
Size 8-17amino acid residues 5-15amino acid residues
or 5-7monosaccharides
Types linear epitope conformational epitope
or linear epitope
Position any position in antigen mostly exist on the surfaceof
antigen

12. Major Histocompactibility complex
(MHC)
.

13. Introduction
13
Major Histocompactibility complex (MHC) is set of surface
proteins located on the cell membrane of nucleated cells.
It plays more important work to indentify the antigen between
SELF AND NON SELF BODY, intracellular
recognization and responsible for antigen presentation.
Histo refers to tissues. Compatibility refers to living together
harmoniously.
MHC molecules always recognize only T lymphocytes.
The two types of MHC are worked in immunity.
T cytotoxic (Tc) cells are recognized by MHC I molecules
T helper (Th) cell recognized by MHC molecules II,
.

14. Definition
14
“Major Histocompactibility complex is membrane attached
protein which work on recognization of antigen between
SELF AND NON SELF BODY AND ANTIGEN
PRESENTATION”.

15. Classes of MHC Molecules
15
The MHC molecules are classified in to four classes namely ;-
1. Class I MHC molecules
2. Class II MHC molecules
3. Class III MHC molecules
4. Class IV MHC molecules

16. Class I MHC Molecules
16
Class I MHC(45 KD) molecule are a group of major
histocompactibility antigen.
They are present on the surface of all nucleated cells
except nervous tissue and platelets.
It present antigen to Tc cells.
It bind with CD-8 adhesion molecules of Tc cells.
It brings about cell mediated immune response.

17. Structure of Class I MHC Molecule
17
It consists two polypeptide chains namely α chain and β2 – micro
globulin.
α chain which is non covalently attached with β2 microglobuline . α chain
contain a transmembrane glycoprotein which is encoded by A,B and C gene
of grouped HLA.
α chain is organized by three domains such as α 1, α 2 and α 3 each domain
containing 90 amino acids sequences .
β2 microglobuline is similar in size of α 3 and it dose not contain trans
membrane proteins .
When the antigen is internalized and processed inside by proteosome
(Ubiquitin, cytosolic degradation), the peptides are produced.
Peptide is further loaded on the groove of MHC I molecules from
endoplasmic reticulum.

18. Peptide
binding
groove
Fig:- Class I MHC antigen
18

19. Class II MHC Molecule
19
Class II MHC molecule are present on the surface of
antigen presenting cell and cell which engulfed the foreign
antigen.
It binds with the exogenous(endocytic degradation )
antigens.
It binds with CD4 adhesion molecules TH cells.
It also consist of two polypeptide chains namely α chain
and β chain.
Antigen is processed inside the endosome and peptide is
further loaded on groove of MHC II molecules.

20. Structure of MHC II Molecule
20
The class II MHC Molecule consists of two polypeptide chain
namely α chain (33 kDa) and β (28kDa) chain.
The both chain are attached noncovelantly.
Each chain contains two units. The two units of α chain are
called α1 and α2. The two domains of β chains are called β1
and β2.
β2 and α2 are transmembrane domains anchoring the MHC to
plasma membrane.
The α1 and β1 domains jointly bear a peptide binding groove.

21. Peptide binding
groove
Fig:- Class II MHC molecule 21

22. Class III MHC molecule
22
The molecules include
complements like C2 and C4 and
Bf (factor B).
Class IV MHC molecule
These molecule is present on T
cells of leukemia(Tla) as well as
on immature thymocytes .

23. HLA - Human Leukocyte Antigen
23
HLA is the human leukocyte antigen.
HLA is the MHC molecules present in human beings.
HLA is a set of surface protein present on the surface of
all nucleated cells. They are responsible for
Graft rejection,
Adaptive immunity,
Defense against infection,
some time it is expressed on cancer cell destruction,
certain autoimmune diseases and certain complements.
MHC is the general term referring to the cell surface
antigen of vertebrates.

24. Function of MHC Molecules
24
MHC molecules are loaded with a bit of sample peptide
fragment derived from the degradation of proteins present
inside the cell. This peptide is the mirror image of proteins
present inside the cell.
MHC molecules contain SELF AS WELL AS
NONSELF (FOREIGN) antigen.
They bring about defense against infections and diseases.
They mediate certain autoimmune diseases.
.

25. Summary
25
The both MHC I and II molecule are responsible for
antigen presentation and it has application of antigen
recognization between self and nonself recognization,
mostly they are located on T lymphocytes encoded by
chromosome 6 of the human.
The two types of antigen degradated peptides
(exogenous and endogenous) are involved to
complete these process of antigen neutralization.

26. Adaptive immunity is
body's ability to
eradicate possibly
harmful foreign
materials or abnormal
cells by developing
specific immune
response against a
particular antigen.
Acquired/Adaptive/Specific Immunity

27. Based on immune response
Humoral & Cellular Immunity
Humoral Immunity
It is a ‘B cells’ generated - antibody mediated immune
response especially effective against bacterial
antigens.
Cellular Immunity
It is a ‘T cells’ mediated immune response especially
effective against intracellular organisms like viruses,
parasites, fungi and others like cancer cells and
transplant cells (few bacterial infection like tubercular
bacilli).

28. Acquired immunity has two components: humoral immunity
and cellular immunity.
Humoral immunity is mediated by B Lymphocytes-
Cellular immunity is mediated by T lymphocytes-
Acquired/Adaptive/Specific
Immunity

29. 2
9

30. The adaptive cell-mediated immune response is initiated by
dendritic cells which have sampled antigen in host tissues
3
0

31. T cell development in the thymus
 T cells develop from progenitors that are
derived from hematopoietic stem cells in
the bone marrow and migrate through
blood to the thymus, where they mature
 T cell development parallels B cell
development in many ways, including
rearrangement of antigen-receptor
genes, sequential testing for successful
gene rearrangement, and the eventual
formation of a complete heterodimeric
antigen receptor
3
1

32. T cells are activated in peripheral
lymphoid organs
• T cells that survive selection mature and
leave the thymus to circulate in the blood
• They repeatedly leave the blood to migrate
through the peripheral lymphoid organs,
where they may encounter their specific
antigen and become activated
3
2

33. Activated T cells become effector cells
 Mature T cells that encounter their
specific (cognate) antigen are
activated
 Activation leads to clonal expansion
and differentiation into effector T
cells, which are attracted to sites of
infection where they can kill infected
cells (CD8+ T cells) or activate
macrophages (CD4+ T cells)
 Other T cells move into B cell-rich
areas of LTwhere they help to
provide an antibody response 3
3

34. 3
4
T cell homeostasis
• T cells which have matured within the thymus for about
1 week emigrate to the periphery
• Relatively small numbers are exported
• In the absence of infection this pool of naïve T cells is
kept at a roughly constant size and composed of diverse
TCR by a regulatory process called homeostasis,
• Hemoestasis involves cytokines - including IL-7 - and
signals received by TCR in response to contact with self-
peptide/MHC.

35. T cell surface MARKER/ receptors
 cluster of differentiation" (CD) nomenclature. This
provided a common nomenclature that allowed the
scientific community to communicate results in a
universal language
 The CD antigen is a protocol used for the
identification and investigation of cell surface
molecules providing targets for immunophenotyping
of cells.
 Recognition of antigen:- CD 3
 Multiple function:- CD 4+
 interactions with antigens- TCR. T cell receptors
 adhesion and binding:- CD8+
 CO STIMULATION :- CD40 L, CD28:-
 adhesion molecule:- CD 2 and LFA 1

36. Activation of naïve T cells requires 3 kinds of signals,
delivered by antigen presenting cells
1. TCR and foreign peptide:MHCII
complex is indicator for activation
2. Co-stimulatory signal eg. CD28 on
naïve T cell and B7 on APC
determines survival for cells which
have been activated by Signal 1
3. Cytokines and other mediators are
released by APC and determine
differentiation pathway and
therefore T cell effector function
CD4+ T cells are shown in this example 10

37. Antigen presenting cells
37
 Dendritic cells are found
throughout the LN cortex in the T
cell-rich areas
 Macrophages are distributed
throughout B cells are found
mainly in the follicles
 The three types of APC are
adapted to present different types
of pathogen or pathogen
products, but mature DC are

38. IL-2 is required for T cell proliferation
38
• Activated T cells secrete and
respond to IL-2
• Activation of naïve T cells in the
presence of costimulation with CD28
induces expression and secretion of
IL- 2, and the expression of high-
affinity
• IL-2 receptors. IL-2 binds to the IL-2R
to promote T cell growth and
proliferation

39. T cells in humoral and cell-mediated immune responses
39

40. 40

41. Effector T cells can respond to their target cells
without costimulation
41

42. Killing by CD8+ cytotoxic T lymphocytes
42
CTLs recognize MHCI-associated
peptides (peptide antigens derived
from intracellular microbes) and
form tight adhesions
(“conjugates”) with these target
cells.
The CTL are activated to release
granules such as granzyme, which
are taken into the target cell and
where they induce apoptosis
(programmed cell death)

43. Summary: The phases of an adaptive immune response
43

44. B-Cell Development, Activation,
and Differentiation
.

45. .
.

46. Overview of B cell development
• B cells are generated in the bone marrow
• Takes 1-2 weeks to develop from
hematopoietic stem cells to mature B cells
• Sequence of expression of cell surface receptor
and adhesion molecules which allows for
differentiation of B cells, proliferation at various
stages, and movement within the bone marrow
microenvironment
• Immature B cell leaves the bone
marrow and undergoes further
differentiation
• Immune system must create a number of
receptors capable of recognizing a large array
of antigens while at the same time eliminating

47. Overview of B cell development
• Early B cell development
constitutes the steps that
lead to B cell commitment
and expression of surface
immunoglobulin,
production of mature B cells
• Mature B cells leave the
bone marrow and migrate
to secondary lymphoid
tissues
• B cells then interact with
exogenous antigen and/or T
helper cells
= antigen- dependent
phase

49. Overview of B cells

50. Mature B cells
• Complete IgM molecule on cell surface
• Mature resting B cells express HLA-DR, CD19, CD20,
CD40
• Exit bone marrow, migrate to secondary lymphoid
organs, then express both surface IgM and IgD as
well as other molecules that mediate cell-cell and
cell-ECM adhesive interactions
• Can recirculate between blood and lymphoid organs,
entering B cell follicles in lymph nodes and spleen,
responding to antigen encounter with T cell help,
leading to antibody production

51. Plasma cells
• Secrete antibodies, have few surface antibodies
• Those that arise from follicular B cells are found mainly
in the bone marrow and are long-lived (months)
• Those that arise from non-follicular B cells are short
lived (days to weeks)
• Plasma cell differentiation involves
– loss of Bcl6, Pax-5, CD19, CD20, and B cell
activation antigens
– Appearance of XBP-1, BLIMP-1, CD38,
CD138, cytoplasmic Ig

53. B CELL SURFACE MARKERS
 B Cell receptors :- Igm, Ig alpha, Ig
beta, CD79A,CD79B
 B cell co receptors:- CD19,CD21,CD 81
 Co stimulating molecules:-
CD40,CD80, B7
 Adhesion molecules:- ICAM 1
 MHC2
 INHIBITORY:- CD22

54. B cell activation
• Exposure to antigen or various polyclonal
mitogens activates resting B cells and stimulates
their proliferation
• Activated B cells lose expression of sIgD and CD21
and acquire expression of activation antigens
– Growth factor receptors, structures involved in cell-
cell interaction, molecules that play a role in the
localization and binding of activated B cells
• Two major types:
• T cell dependent (TD) a
• T cell independent (TI)

55. B cell activation
• Two major types:
• T cell dependent (TD) a
• T cell independent (TI)
• TD: involves protein antigens and CD4+ helper T cells
– 1) Multivalent antigen binds and crosslinks
membrane Ig receptors
– 2) Activated T cell binds B cell thru antigen
receptor and via CD40L (T)/CD40 (B) interaction
• TI: involves multivalent or highly polymerized
antigens, does not require T cell help
– TI-1:- LPS. Mitogenic at high concentrations to most
B cells because of binding to pattern recognition
receptors (PRRs) on B cell surface. At low
concentrations, only activates those B cells that bind
the antigen via the Ig receptor
– TI-2:- bacterial capsular polysaccharide. Highly
repetitive antigens. Not mitogenic but can crosslink Ig
receptors. Many are bound by C3d.

56. B cell activation
• Following TD antigen activation, some activated B cells
differentiate into plasma cells in primary foci that are outside
of the follicles, then migrate to the medullary cords of the
lymph node or to the bone marrow. Secrete IgM within 4
days.

58. B cell activation
• Other activated B cells enter the follicle, divide and differentiate;
germinal centers form.
• Within the germinal center, Ig genes undergo class switching: the
 constant regions replaced by other constant regions and the
variable region is subject to somatic hypermutation.
• Mutated variable region subject to antigen-mediated selection
• Low affinity and autoreactive B cells die while those with
improved affinity leave the germinal centers.
• Antibodies with mutations in the variable region appear in the
circulation within 6-10 days

60. T-dependent B-Cell Response
• At conclusion of primary immune response, two sets
of long-lived cells remain:
– Memory B cells
• On secondary exposure to the same
antigen, the memory B cells will be
stimulated and result in production of high-
affinity, heavy-chain class- switched
antibodies
– Plasma cells
• Majority of the expanded population of antigen-
specific B cells undergo apoptosis

61. Clonal Selection
Only one type of
antibody—and one
type of B cell—
responds to the
antigenic determinant
That cell type
then produces a
large number of
clones
Dr Ashwani
kumar
61

62. Class switching Gene rearrangement
 The process of synthesis of immunoglobulin's by B
lymphocytes involve permanent rearrangement of
the DNA of these cells
 There are approx. 300variable (V),5 joining gene
(J),and 10 diversity (D) genes
 During development of B lymphocytes single (V)
(D) and joining gene segments are brought
together through gene rearrangement to form a
unique variable region
 This allow generation of 109-1011 different
immunoglobulin from a single gene needed for 62

63. GENE rearrangement
63

64. Class switching
• Influenced by cytokines
– IL-4  IgG1, IgE
– TGF-  IgA, IgG2b
– IL-5  IgA
– IFN-  IgG3, IgG2a

65. Primary (naïve) vs Secondary
(memory) B cells
Naïve Memory
Lag period after antigen
exposure
4-7 days 1-3 days
Time of peak response 7-10 days 3-5 days
Magnitude of peak
antibody response
Variable 10-1000 times higher than
primary response
Antibody isotype IgM IgG (IgA in mucosal tissues)
IgM/IgD expression Positive/positive Mostly negative/negative
Antibody affinity Low High
Life span Days to weeks Long-lived
Recirculation Yes Yes

66. Summary of thymus-dependent vs
thymus-independent antigens
TD antigens TI type I antigens TI type 2 antigens
Antigen type Soluble
protein
Bacterial cell wall
components (e.g.,
LPS)
Polymeric protein
antigens, capsular
polysaccharides
Humoral response
Isotype switching
Affinity maturation
Immunologic memory
Polyclonal activation
Yes
Yes
Yes
No
No
No
No
Yes (high doses)
Limited
No
No
No

67. 67
ANTIBODIES/immunoglo
bulins?
• Antigen specific proteins produced
by plasma cells
• Belong to immunoglobulin superfamily
• Located in blood and extravascular
tissues, secretions and excretions
• Bind pathogenic microorganism and their
toxins in extracellular compartments
• Secreted form of immunoglobulin's

68. Antibodies
Antibodies are assembled out of
protein chains.
There are many different chains that
the immune system assembles in
different ways to make different
antibodies.

69. 2 identical heavy chains
2 identical light chains
Each heavy chain – has a
constant and a variable
region and each light chain
has a constant and a
variable region.
Fab – fragment antigen
binding site,
Fc- Fragment complement
and some immune cell
binding site.
Antibody- Basic Structure
Constant
region
Variable
region
L L
H H

70. Dr.Ashwanikumar 70
.

71. CLASSES (ISOTYPES) OF IMMUNOGLOBULINS
• Classes based on constant region of heavy chains
– Immunoglobulin A (IgA)
– Immunoglobulin D (IgD)
– Immunoglobulin E (IgE)
– Immunoglobulin G (IgG)
– Immunoglobulin M (IgM)
• Differentiation of heavy chains
– Length of C region, location of disulfide bonds, hinge
region, distribution of carbohydrate
• Classes have different effector functions
Dr.Ashwani
kumar
71

72. Different classes of Antibodies
Dr.Ashwani
kumar 72

73. Humoral Immunity - Effector Phase-Antibodies

74. Immunoglobulin Classes
I. IgG
Structure: Monomer
Percentage serum antibodies: 80%
Location: Blood, lymph, intestine
Half-life in serum: 23 days
Complement Fixation: Yes
Placental Transfer: Yes
Known Functions: Enhances
phagocytosis, neutralizes toxins and
viruses, protects fetus and newborn.
Dr.Ashwani
kumar
74

75. Immunoglobulin Classes
II. IgM
Structure: Pentamer
Percentage serum antibodies: 5-10%
Location: Blood, lymph, B cell surface (monomer)
Half-life in serum: 5 days
Complement Fixation: Yes
Placental Transfer: No
Known Functions: First antibodies produced
during an infection. Effective against microbes
and agglutinating antigens.
Dr.Ashwani
kumar
75

77. Immunoglobulin Classes
III. IgA
Structure: Dimer
Percentage serum antibodies: 10-15%
Location: Secretions
(tears, saliva, intestine, milk), blood and lymph.
Half-life in serum: 6 days
Complement Fixation: No
Placental Transfer: No
Known Functions: Localized protection of
mucosal surfaces. Provides immunity to infant
digestive tract. Dr Ashwani
kumar
77

79. Immunoglobulin Classes
IV. IgD
Structure: Monomer
Percentage serum antibodies: 0.2%
Location: B-cell surface, blood, and lymph
Half-life in serum: 3 days
Complement Fixation: No
Placental Transfer: No
Known Functions: In serum function is unknown.
On B cell surface, initiate immune response.
Dr Ashwani
kumar
79

80. Immunoglobulin Classes
V. IgE
Structure: Monomer
Percentage serum antibodies: 0.002%
Location: Bound to mast cells and basophils
throughout body. Blood.
Half-life in serum: 2 days
Complement Fixation: No
Placental Transfer: No
Known Functions: Allergic reactions. Possibly
lysis of worms.
Dr Ashwani
kumar
80

81. Timing of memory immune response
• Primary response
– Lag period: division/differentiation of B cells
within the primary foci, movement into
germinal center
– B cells of primary foci release IgM
– B cells that have migrated into the germinal
center release IgM and IgG
– Somatically hypermutated receptors appear,
select population of B cells leaves the germinal
center and enters the memory B cell
compartment

82. Secondary response
– Expanded set of memory B cells with high-
affinity receptors are available for
immediate differentiation to high- affinity
IgG secretion
– Somatically hypermutated B cells can
undergo further hypermutation with
additional antigen exposure, increasing the
average affinity of the antigen-specific
antibodies

85. Role of antibodies
Antibodies released into the blood stream will bind to the antigens
that they are specific for.
Antibodies may disable some microbes, or cause them to stick
together (agglutinate). They “tag” microbes so that the microbes
are quickly recognized by various white blood cells.

86. Antigens as Effectors
Free antibodies can bind to
antigens, which “tags” the
antigen for the immune system
to attack and destroy.

87. Antibodies as Receptors
Antibodies can attach to B cells,
and serve to recognize foreign
antigens.

88. Thank you

89. Dr Ashwani
kumar
89
Immunological Memory
Antibody Titer: The amount of antibody in the
serum.
Pattern of Antibody Levels During Infection
Primary Response:
– After initial exposure to antigen, no antibodies
are found in serum for several days.
– A gradual increase in titer, first of IgM and then
of IgG is observed.
– Most B cells become plasma cells, but some B
cells become long living memory cells.
– Gradual decline of antibodies follows.

90. Immune system
Bone
Marrow
Acquired
Immune
system

91. Cell mediated immunity
•Immunity against infections
•Rejection of allograft
•Tumour cell destruction
•Helper function
•Supressor function
•Production of lymphokines
•Delayed type hypersensitivity

93. Mechanism of action of antibodies
•Classical complement pathway
•Antibody-dependent cell mediated
cytotoxicity
•Agglutination
•Opsonization of target cells

94. Events between entry of ag, its processing and
presentation by antigen presenting cells
(Macrophages/B cells) to helper T cells.
▪ Ingestion of Ag
▪ Enzymatic degradation of
Ag
▪ Presentation of theses
processed Ag (epitopes)
in association with MHC II to
Helper T cells (TH2) or CD4
cells.
1)TCR are surrounded by Adhesion protein to clomplementary proteins of APC12) Processed Ag to TCR MHCII –Immunogenic synapse.
(TH2)

95. Clones of B cells recognize
antigens (Clonal Selection)
through the TH2, Gets activated by
the released cytokines
Differentiate into plasma cells and
memory cells→The
immunoglobulins are secreted
.

96. Immunological Memory (Continued)
Secondary Response:
– Subsequent exposure to
the same antigen displays
a faster and more intense
antibody response.
– Increased antibody
response is due to the
existence of memory
cells, which rapidly
produce plasma cells upon
antigen stimulation.
Dr Ashwani
kumar
96

97. Self Assessment
Humoral immunity is mediated by ……………… lymphocytes.
Cellular immunity is mediated by ………….. …. lymphocytes.
………………… fragment of antibody is antigen binding site.
……………………fragment of antibody is complement and some immune cell binding site.
Presentation of theses processed Ag occurs in association with ……………………….to
Helper T cells.

98. Dynamics of Antibody Production
Latent period
– Gradual rise in
antibody
production taking
days to weeks
– Plateau reached
– Antibody
level
declines Dr Ashwani
kumar
98

99. Secondary Response
• Second exposure to
SAME antigen.
• Memory cells are
a beautiful thing.
• Recognition of antigen
is immediate.
• Results in immediate
production of
protective antibody,
mainly IgG but may
see some IgM
. 99

100. Humoral Immunity – Action of B-Memory Cells

101. Dynamics of Antibody Production
Dr Ashwani
kumar
10
1
• Antibody production
– Initial antibody produced in IgM
– Lasts 10-12 days
– Followed by production of IgG
– Lasts 4-5 days
– Without continued antigenic challenge
antibody levels drop off, although IgG may
continue to be produced.

102. • In the secondary immune
response
– Memory cells facilitate a faster, more efficient
response
Antibody
concentration
(arbitrary
units)
104
103
102
101
100
0 7 14 21 42 49 56
28 35
Time (days)
Antibodies
to A
Antibodies
to B
Primary
response to
antigenA
produces anti-
bodies toA
2
1 Day 1: First
exposure to
antigenA
3 Day 28:
Second exposure
to antigenA; first
exposure to
antigen B
4 Secondary response to anti-
genA produces antibodies
to A; primary response to anti-
gen B produces antibodies to B
Dr Ashwani
kumar
10
2

103. THE PRIMARY HUMORAL IMMUNE
RESPONSE
Dr Ashwani
kumar
10
3
• Immune response initially produces IgM
antibodies then switches to IgG
antibodies
• Question
– Why switch from IgM to IgG?
• Answer
– Limited effector mechanisms for IgM
– Range of effector mechanisms for IgG
• Mechanism
– Isotope or class switching