1. The Adaptive Immune Response
Specific Defense
The Adaptive Immune Response

2. Specific Immunity Augments mechanisms of nonspecific defense
Has memory about specific pathogens
Second encounter with same pathogen
B lymphocytes –humoral immunity
T lymphocytes-cell mediated immunity

3. 3rd Line of Defense Acquired immunity-develops over lifetime
Naturally acquired active immunity
Exposed to microbe

4. Acquired Immunity Naturally acquired passive immunity
Antibodies from mother
Placenta -IgG
Colostrum-IgA

5. Artificially Acquired Immunity
Active-vaccines
Live attenuated vaccines-mutated microbes
Serial passage in cell cultures
Adaptation to low temperatures-25 C

6. Artificially Acquired Immunity
Inactivated or killed vaccines
Non infective
Lower immune response
Passive- immune serum
Lasts few weeks to months
Destroyed by host

7. Antigens Immunogens-provoke an immune response
Most proteins or polysaccharide
Larger the molecule the better the immune response
Foreign molecules usually or “nonself”
Components of microbes
Food allergens
Dust-microbes, pollen etc.

8. Properties of Antigens
3 dimensional shapes of regions where antibody binds
Antigenic determinants or epitopes
Stimulate immune response 6-8 aa or monosaccharides
Larger more complex molecules are better antigens
Haptens-small molecules-hormones, peptides

9. Types of Antigens Exogenous antigens Endogenous antigens
Microbes reproduce within cells
Immune response occurs only if

10. Types of Antigens Autoantigens Antigens found on normal cells
Immune response against oneself
Leads to inflammation of tissues-lupus

11. Lymphocytes Produced in red bone marrow-2 types
B lymphocytes
T lymphocytes
Based upon surface glycoproteins-CD4, CD8
T lymphocytes mature in thymus
Self T cells undergo apoptosis
B lymphocytes mature in bone marrow
Found mainly in spleen, lymph nodes ,bone marrow
Circulate in blood

12. Antibodies
Proteins made in response to antigen by B cells-plasma cells
Ig or antibodies part of humoral response
Bind to a specific antigen
Most effective before microbe, toxin enters cells
Measure antibody titer -quantity of antibody needed to produce a reaction
Detectable with specific antigen

13. Immunoglobulins (IgGs)
Structure
Bivalent antibody-monomer
2 antigen binding sites
4 peptide chains
2 light chains and 2 heavy (longer) chains
Joined together by disulfide bonds
Molecule looks like letter Y

14. Structure Stem of antibody-Fc region
Lower portions of heavy chains
Only 5 types of heavy chains
5 classes of antibodies named from chain
Fc regions of adjacent abs bound to microbe can bind complement and destroy organism

15. V-Variable Regions
Arms of heavy & light chains vary in amino acid sequences from one B cell to another
Same for every antibody produced by that B cell
Area that forms antigen binding site
Fab regions

16. Immunoglobulin Classes
IgG
protect against circulating bacteria and viruses
neutralizes bacteria toxins
triggers complement
when bound to ag , enhances phagocytosis
cross placenta and instill passive immunity to fetus

17. IgM Stays in blood and lymph Involved in ABO blood group ags response
Reacts with C, enhances phagocytosis
First ab to respond to initial ag

18. IgM Used in diagnosis of disease Does not cross placenta
IgM indicates acute infection
IgG past infection
Does not cross placenta

19. IgA Most common in mucus membranes and body secretions
In all, most abundant in body
Secretory IgA is dimer,2 monomers connected by J chain

20. IgA Function-prevent attachment of pathogens to mucosal surfaces
IgA immunity is short lived so respiratory infections’ immunity not long
Found in colostrum
Does not cross placenta
Does not activate complement

21. IgD 0.2% of abs Found in blood and lymph and on surface of B cells
Act as antigen receptor on B cells
Initiates the immune response
Does not activate complement

22. IgE Low concentration in serum
Not important in neutralization, opsonization or agglutination
Acts as signal molecule
Attaches to receptors on basophils, mast cells
Trigger release of histamine-inflammation
Important in allergic responses
Also on eosinophils-parasites

23. Humoral Immunity Antibody mediated immunity
B cell exposed to extracelluar antigens
Becomes activated-differentiates into clone of plasma cells
Produce antibodies
T helper cells activate B cells
T dependent antigens

24. T-Dependent Antigens Processing of exogenous antigens (protein)
Antigen determinant binds with MHC molecules in a vesicle
Complex inserted in CM with antigen presented on outside of B cell
Activated T helper cells binds to antigen

25. Clonal Selection B cell binds antigen
Proliferates into clone with same receptor on surface
If T dependent antigen (proteins), T helper cell will activate B cell to produce plasma cells
Some become memory cells for long term immunity
Self tolerance
B & T cells that react with self antigens removed during early development

26. T-Independent Antigen
B cells can bind directly to large antigens –capsule ( CH2O )
Initiate clonal expansion
T cells not always activated & T cell memory may not occur
Small antigens such as viruses
B cells need help from helper T cells

27. Secondary Immune Response
On second encounter with antigen
Population of memory cells will proliferate and differentiate into plasma cells
No need for APCs
Get a rapid and effective response

28. Memory Cells
Long lived cells with BCRs complementary to specific ag determinant
Can survive months or years
Primary response-abs produced slowly
May survive for months or more
Ends when plasma cells die

29. Apoptosis Programmed cell death Rid body of excessive B & T cells etc.
Prevent leukemia
Rid of self cells without eliciting inflammation

30. Antibody Function Ag binding sites complementary to antigens
Antigen binds to antibody
Results in activation of complement, stimulation of inflammation, cytolysis, & phagocytosis-nonspecific
Results in agglutination, neutralization & opsonization

31. Mechanisms of Inactivation
Agglutination-cause ags to clump together
IgM is more effective because of many binding sites

32. Mechanisms of Inactivation
Neutralization
IgG abs inactivate viruses by blocking attachment to host cells
Neutralize bacterial toxins by blocking active site on toxin (antitoxin)
Toxin or microbe can’ t bind to target cells

33. Mechanisms of Inactivation
Opsonization
ag such as bacterium is coated with abs that enhance its ingestion and lysis by phagocytic cells
Neutrophils & macrophages have receptors for Fc region of antibodies

34. Cell Mediated Cytotoxicity
Antibody dependent: target cell is coated with antibodies
NK, macrophages, neutrophils and eosinophils will bind to Fc of antibodies
Cells especially eosinophils release chemicals that lyse large pathogens

35. Types of T Cells Helper T Cells: CD4 glycoprotein
Cytotoxic T cells: CD8
Antigen presented on surface of antigen presenting cells (APC)
Macrophages & dendritic cells

36. T Lymphocytes
In thymus each T cell generates multiple copies with specific T cell receptor
TCR has 2 different polypeptide chains with groove between
Antigen binding site
Act directly against endogenous invaders
Do not secrete Ig but produce cell mediated immune response
Antigen must be presented by host cell

37. Helper T Cells Help in regulating activity of B cells and T cells
2 types-TH1 & TH2
TH1’s cytokines assist cell mediated immunity: cytotoxic T cells, macrophages & NK cells
TH2’s cytokines activate B cells
Assist antibody mediated immunity
T dependent antigens

38. Cytotoxic T cells Leave lymphoid tissue & go to infected site
Destroy infected cells upon contact
Antibodies cannot attack infected cells
T cell binds to MHC-antigen on cell
Releases perforin forms pore in cell
Cell lyses, afterwards apoptosis occurs