lymphocytes notes

1. ADAPTIVE IMMUNE
SYSTEM

2. STRATEGY OF ADAPTIVE
IMMUNE RESPONSE
 First response to particular antigen called
primary response
 May take a week or more to develop
 Immune system remembers pathogen on
subsequent exposure
 Termed secondary response
 Adaptive immunity divided into
 Humoral immunity
 Eliminates extracellular pathogens
 Cellular immunity
 Eliminates intracellular pathogens

3. HUMORAL IMMUNITY
B LYMPHOCYTE
 Overview of humoral immunity
 Mediated by B lymphocytes
 a.k.a B cells
 Develops in bone marrow
 B cells may be triggered to proliferate into plasma
cells
 Plasma cells produce antibodies
 Antibodies produce when antigen bonds B cell receptor
 Some B cells produce memory cells

4. Nature of Antigens
 Coined from compounds that elicit antibody
production
 Antibody generator
 Includes an enormous variety of materials
 Today, term used to describe any compound
that elicits an immune response
 Antigen that causes immune response termed
immunogen
 Proteins and polysaccharides induce string
response
 Lipids and nucleic acids often do not
 Recognition of antigen directed at antigenic
determinant or epitope

5. Nature of Antibodies
 Structure of the Antibody (Ab)
 Basic Y-shaped structure
 Made of four chains of amino acids held together by disulfide bonds
 Two chains are heavy
 Two chains are light
 Each heavy and light chain has a constant region
 The constant region is known as Fc region
 Each heavy and light chain has a variable region
 Variable region is unique to each Ab
 This region binds to a specific Antigen and is known as “Fab”
region

6. Nature of Antibodies
 Protective outcomes of antibody-antigen
binding
› Neutralization
 Prevents toxin from interacting with cell
› Immobilization and prevention of adherence
 Antibody bonding to cellular structures to interfere with
function
› Agglutination and precipitation
 Clumping of bacterial cells by specific antibody
 Bacteria more easily phagocytized

7. Nature of Antibodies
 Protective outcomes of antibody-antigen
binding
› Opsinization
 Coating of bacteria with antibody to enhance phagocytosis
› Complement activation
 Antibody bonding triggers classical pathway
› Antibody-dependent cellular cytotoxicity
 Multiple antibodies bind a cell which becomes target for
certain cells

9. Nature of Antibodies
 IgM
 First Ab to respond to infection
 5 – 13% of Ab in circulation
 Only Ab that can be formed by the fetus
 IgM expressed as membrane bound anitbodies on B-cells
 Pentamer
 5 units held together by disulfide bonds
 J (Joining) chain functions in the polymerization of monomers
 First immunoglobulin class produced in a primary response to an antigen
 Has 10 anitgen binding sites
 More effective at stimulating complement
 Large-size - does not diffuse well
 The FC receptors on phagocytes bind IgM (opsinization)

10. IgM

11. Nature of Antibodies
 Five classes of Ab
IgG
 Dominant Ab in circulation
• 80 – 85% Ab in circulation
 Structure = monomer
 The antibody of memory!!!!!
 Cross placenta and play important role in protecting
fetus
 Provides passive immunity to unborn fetus.
 Placental cells bind the Fc portion of IgG and transfer Ab
across the placental membrane.
 Activate complement system
 Opsonin—phagocytosis

12. IgG

13. IgA
 Found in secretions
 10 - 13 % of Ab in circulation
 Found Predominantly in external secretions i.e. Breast Milk,
Saliva, tears, mucus.
 Serum form is a monomer
 Plasma cells that release IgA Abs are concentrated along the
Mucus Membrane surface.
 Provides passive immunity to infants through mothers breast
milk

14. Secretory IgA

15. Nature of Antibodies
 Five classes of Ab
 IgD
 <1% of total Ab in circulation
 Structure = monomer
 Maturation of antibody response
 Despite studies extending for more than 4 decades, a
specific role for serum IgD has not been defined
while for IgD bound to the membrane of many B
lymphocytes, several functions have been proposed.
 Does NOT cross the placenta.
 Does NOT fix complement.

16.  Ig E
Barely detectable in circulation
Active in allergic reaction
 Mediate the immediate hypersensitivity reactions
(hayfever, asthma, hives, anaphylactic shock)
 Mast cells and basophils bind fc portion of IgE
 Cross-linkage of receptor bound IgE molecules by antigen,
induces degranulaltion of the Mast and basophil cells
 Parasitic response
 Eosinophils express receptors for IgE

17. IgE

18. CELL MEDIATED
T LYMPHOCYTES
 Overview of cellular immunity
 Mediated by T lymphocytes
 a.k.a T cells
 Matures in thymus
 Divided into 2 subsets
 Cytotoxic T cells
 Helper T cells
 T cell receptors help with antigen recognition

19.  Two major function T cell populations
 Cytotoxic T cells
 Proliferate and differentiate to destroy infected or
cancerous “self” cells
 Have CD8 marker
 Recognize MHC class I
 Helper T cells
 Multiply and develop into cells that activate B cells and
macrophages
 Stimulate other T cells; orchestrate immune response
 Have CD4 marker
 Recognize antigen display by MHC class II

20.  During antigen presentation, antigen cradled in
grove of major histocompatability complex
molecule (MHC molecule)
 Two types MHC
 MHC class I
 Bind endogenous antigen
 MHC class II
 Bind exogenous antigen

21. NATURAL KILLER CELLS
 Natural killer cells descend from lymphoid stem
cells
› They lack antigen specificity
 No antigen receptors
 Recognize antigens by means of Fc portion of IgG antibodies
 Allow NK cells to attach to antibody-coated cells
 Actions augment adaptive immune response
› Important in process of antibody dependent cellular
toxicity
 Enable killing of host cells with foreign protein in membrane
 Natural killer cells recognize destroyed host cells
with no MHC class I surface molecules
› Important in viral infection

22.  Role of T cells different from B cells
 T cells never produce antibodies
 T cells armed with effectors that interact directly
with antigen
 T cell receptor does not react with free antigen

23. Harmful effects of Immunity
1. AUTOIMMUNITY
It may be defined as the failure of normal process
of an individual to distinguish between self and
non-self i.e when the individual fails to recognize
its own parts as self and develops an immune
response against its own cells and tissues.
Diseases that occur because of autoimmunity are
called as autoimmune diseases.

24.  They result in structural and functional damages
to the host they include
1. Autoimmune hemolytic anemia
2. Thyrotoxicosis( graves disease)
3. Myasthenia gravis
4. Rheumatoid arthritis

25. 2.HYPERSENSITIVITY
 Hypersensitivity diseases or ailments caused by
impaired immune responses are called
hypersensitivity disorders.
The Causes of hypersensitivity diseases are
 Autoimmunity
 Reactions against microbes
 Reactions against environmental antigens

26. Reactions against microbes
 Reactions against persistent microbial agent may
occur in the form of T-cell response.
Tuberculosis, inflammatory bowel disease and
viral hepatitis are some of the related conditions.

27. Reactions against environmental antigens
 It does not occur in majority of the population
but very less percentage of the individuals may
show reaction against some harmless
environmental products. As a result of allergy
such patients generate immunoglobulin E (IgE)
antibodies that cause allergic reactions or
disease.

28. Mechanism and classification of
hypersensitivity reactions
 Based on immune response and some
miscellaneous factors, hypersensitivity reactions
are classified as follows
1. Type I hypersensitivity or immediate
hypersensitivity
 It is characterized by the stimulation of helper T
cells that are associated with production of IgE
antibodies and inflammation. Type I is the most
common hypersensitive reaction. Atopy or
allergic reaction is the best example of type I
reactions.

29. 2.Type II hypersensitive disorders
 This occurs due to activation of complement
system by IgG and IgM antibodies. Some of these
antibodies are specific for some antigens and the
disease caused by such antibodies are called type
II hypersensitive disorders such as Graves’
disease.

30. 3.Type III hypersensitive disorders
Various other antibodies make immune
complexes in blood circulation and cause tissue
damage. Such immune complex diseases are
called type III hypersensitive disorders. Arthus
reaction is a type III hypersensitive disorder.

31. 4.Type IV hypersensitive disorder/Delayed
hypersensitivity
 It involves activation of phagocytes, T-
lymphocytes, and natural killer cells. Multiple
sclerosis is one of such kind.
 In brief, majority of hypersensitive reactions are
caused by stimulation of subset of T helper cells.
 They generally induce inflammation and tissue
damage by recruiting neutrophils and
macrophages

32.  Activated T cells do one of two things:
• release cytokines that activate macrophages, or
• kill cells directly
 This process is normally useful against intracellular organisms
(viruses, fungi, parasites)
 Here, it causes bad stuff: inflammation, cell destruction,
granuloma formation