1. 17
Adaptive Immunity: Specific Defenses of the Host

2. Student Learning Outcomes
Differentiate between innate and adaptive immunity, and humoral and cellular immunity.
Define antigen, epitope, and hapten.
Explain the function of antibodies and describe their structural and chemical characteristics. Name one function for each of the five classes of antibodies.
Compare and contrast T-dependent antigens and T-independent antigens.
Differentiate between plasma cell and memory cell.
Describe clonal selection.
Describe four outcomes of an antigen-antibody reaction.
Differentiate between helper T and cytotoxic T
Define apoptosis.
Define antigen-presenting cell.
Describe the role of antibodies and natural killer cells in antibody-dependent cell-mediated cytotoxicity.
Identify at least one function of each of the following: cytokines, interleukins, interferons.
Distinguish a primary from a secondary immune response.
Contrast the four types of adaptive immunity.

3. Immune System Overview
Def. of innate immunity: __________________
Adaptive immunity: “Ability of the body to react to specific microbial infection”.
Adaptive immunity is….
ag specific and has ______________
made up of two branches
____________ Immunity (B cell mediated)
____________ Immunity (T cell mediated)
integrated with _______________
has ability to ignore healthy “self” molecules (tolerance)

4. Vocabulary
Antigen (ag): Molecule (or part of molecule) that initiates production of specific antibodies or sensitized T cells.
Antibody (ab): Proteins made in response to an ag; can bind to that ag. Other names: __________________, _________________
Serology: Study of reactions between abs and ags in vitro.
Antiserum: Blood-derived fluid containing abs.
Complement:

5. Serum Proteins
Fig 17.19

6. The Nature of Antigens Antigens and antigenic Determinants
Antibodies recognize and react with parts of antigens known as antigenic determinants or epitopes
Fig 17.1

7. Hapten
Definition: Small molecule not antigenic by itself. Becomes antigenic when bound to “carrier molecule”
Fig 17.2
Some drugs, esp. (?) _________________________

8. The Nature of Antibodies
Immunoglobulin Structure: 4 polypeptide chains (2 heavy and 2 light)
Variable regions
Constant regions
Fig 17.3
Fig 17.3

9. 5 Immunoglobulin Classes: G, M, A, E, D
Monomers (bivalent)
80% of serum abs
Protect fetus and newborns (how?) _______________________
Activate complement
Act as opsonins (_____________________)
Neutralize toxins and viruses;
Half-life = 23 days
IgG

10. IgM Pentamer aggregates (too big to move freely) 5-10% of serum abs
Good at causing clumping of ags (= ______________)
1st ab produced in response to infection
Half-life = 5 days (short! – good for use in diagnostics!)

11. IgA
Dimer aggregates
Most abundant in body, especially in secretions (?)
Mucosal protection  prevents ___________

12. IgD
IgE
Monomers
Mostly on surface of virgin B cells  initiate immune response
Monomers
Produced by B cells, but bind to mast cells and basophils
 Degranulation (?) when IgE binds to ag
Useful in parasitic infections (e.g.:________)
Annoying in allergies

13. B cells and Humoral Immunity
Effective against free or extracellular antigens, such as
_____________
B cell receptors (mostly IgM and IgD)
After clonal selection  clonal expansion leading to
Plasma cells (effector cell for antibody production) and
Memory cells

14. Clonal Selection and Clonal Expansion
Fig 17.5
Mastering: Humoral Immunity – Clonal Selection and Expansion

15. Response to T – dependent antigens
B cells require help of T cells for most protein antigens (T-dependent ags)
B cells internalize antigen and present it to T-helper cell in combination with MHC class II molecules
If T cell recognizes antigen it activates B cell  clonal expansion  plasma cells and memory cells
Fig 17.4

16. Response to T – Independent Antigens
No T-helper cells involved
Polysaccharides (bacterial capsules) and LPS
Weak response with no memory cells
Young children react poorly
Fig 17.6

17. Antigen—Antibody Binding & its Results
Affinity: __________of bond between ag and ab.
Specificity: Ab recognizes a specific epitope.
Agglutination and precipitation
Opsonization
Neutralization (to immobilize and prevent adherence)
Complement activation
ADCC: Antibody-Dependent Cell-mediated Cytotoxicity via NK cells and eosinophils
 Protective outcome: Disposal of antigen

18. 5 Protective outcomes of ag-ab binding The Results of ag-ab Binding
Review next slide
ADCC
The Results of ag-ab Binding
Fig 17.7

19. T Cells and Cellular Immunity
Compare to
Fig 17.10
T cells have specific TCR on surface.
TCR does not recognize free antigen. Ag must be presented in association with MHC II on an antigen-presenting cell (APC).
Antigens are processed by APC and positioned on the surface of the APC.

20. Fig 17.10
Activation of CD4+T helper cells

21. Classes of T cells T Helper Cells (TH, CD4+)
Activated by APC with MHC-II.
Starts to secrete cytokines activating other T cells and B cells
Co-stimulatory signal necessary: TLRs
T Cytotoxic cells (TC, CD8+)  CTL (= effector cell) when activated)
Target cells are self-cells carrying endogenous antigens
Activated into cytotoxic T lymphocytes (CTLs)
CTLs recognize Ag + MHC I
Induce apoptosis in target cell
CTL releases perforin and granzymes

22. Antigen Recognition by T Cells
MHC Class I on all nucleated cells
Antigen Recognition by T Cells
MHC Class II on surface of APCs (Macrophages, B-cells, dendritic cells)

23. Apoptosis in target cell
Mechanism of Action of CTL: Destruction of cells displaying MHC-I-Ag complexes
Perforin forms pores
in target cell membrane
Granzymes enter and trigger
Apoptosis in target cell
Similar but different from MAC !!
Fig

24. APCs
Three major types:
__________________
Digest antigen
Present ag fragments on surface in connection with MHC-II molecule
Th-cells recognize ag-MHC-II complex
Mastering: T Cell-mediated Immunity – Helper T Cells

25. Natural Killer (NK) Cells
10 – 15% of circulating lymphocytes
Not immunologically specific  part of _______
Kill target cell if MHC-I absent, e.g.:
Some transformed cells
Some virus infected cells, esp. early infection stage
Large extracellular parasites
Similar mechanism to CTLs: Pore formation, then apoptosis or lysis
Colored SEM; NK cells attacking a cancer cell. (Karolinska Institute)

26. Immunological Memory
Amount of abs in serum is called the antibody titer.
1st contact with an ag  1 response  1st ab?
Subsequent contact with same ag  2 response  Rapidly very high antibody titer. Mostly _____.
Is immunological memory good for ever?
Fig 17.17

27. Types of Adaptive Immunity
Active immunity
Protection via introduction of antigen into responsive host, e.g.:
Naturally acquired via ___________ or
Artificially acquired via ___________

28. Passive Immunity
Protection via transfer of antibodies or immune cells into a non-immune host, e.g.:
Naturally acquired:
Artificially acquired: injection of immune serum
Snake bite
Rh+ child with Rh- mother
Treatment of infectious diseases (??)

29. Compare to
Fig 17.18

30. The End Foundation Fig 17.20: Summary of Adaptive Immunity
Immunology Micro Flix
The End