17Adaptive

Immunity: Specific

Defenses of the Host

Student Learning OutcomesDifferentiate 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.

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

1. ____________ Immunity (B cell mediated)2. ____________ Immunity (T cell mediated)

integrated with _______________ has ability to ignore healthy “self” molecules

(tolerance)

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:

Serum Proteins

Fig 17.19

Antibodies recognize and react with parts of antigens known as antigenic determinants or epitopes

Fig 17.1

Antigens and antigenic Determinants

The Nature of Antigens

HaptenDefinition: Small molecule not antigenic by itself.

Becomes antigenic when bound to “carrier molecule”

Some drugs, esp. (?) _________________________

Fig 17.2

The Nature of Antibodies

Fig 17.3

Immunoglobulin Structure: 4 polypeptide chains (2 heavy and 2

light) Variable regions Constant regions

Fig 17.3

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

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!)

IgM

Dimer aggregates

Most abundant in body, especially in secretions (?)

Mucosal protection prevents ___________

IgA

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

Monomers

Mostly on surface of virgin B cells initiate immune response

IgD

IgE

B cells and Humoral ImmunityEffective against free or extracellular antigens, such as

1. _____________

2. _____________

3. _____________

B cell receptors (mostly IgM and IgD)

After clonal selection clonal expansion leading to

4. Plasma cells (effector cell for antibody production) and

5. Memory cells

Clonal Selectionand Clonal Expansion

Fig 17.5

Mastering: Humoral Immunity – Clonal Selection and Expansion

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

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

Antigen—Antibody Binding & its Results Affinity: __________of bond between ag and ab. Specificity: Ab recognizes a specific epitope.

1. Agglutination and precipitation

2. Opsonization

3. Neutralization (to immobilize and prevent adherence)

4. Complement activation

5. ADCC: Antibody-Dependent Cell-mediated Cytotoxicity via NK cells and eosinophils

Protective outcome: Disposal of antigen

Fig 17.7

The Results of ag-ab Binding

5 Protective outcomes of ag-ab binding

Review next slide

ADCC

T Cells and Cellular Immunity

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.

Compare to Fig 17.10

Fig 17.10

Activation of CD4+T helper cells

Classes of T cellsT Helper Cells (TH, CD4+)

Activated by APC with MHC-II. Starts to secrete cytokines activating other T cells and B cellsCo-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

MHC Class I on all nucleated cells

MHC Class II on surface of APCs (Macrophages, B-cells, dendritic cells)

Antigen Recognition by

T Cells

Mechanism of Action of CTL: Destruction of cells displaying MHC-I-Ag complexes

Perforin forms poresin target cell membrane

Granzymes enter and trigger

Apoptosis in target cell

Fig. 17.12Similar but different from MAC !!

APCsThree major types: 1.__________________

2.__________________

3.__________________

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

Natural Killer (NK) Cells

10 – 15% of circulating lymphocytes

Not immunologically specific part of _______

Kill target cell if MHC-I absent, e.g.: 1. Some transformed cells

2. Some virus infected cells, esp. early infection stage

3. Large extracellular parasites

Similar mechanism to CTLs: Pore formation, then apoptosis or lysis

Colored SEM; NK cells attacking a cancer cell. (Karolinska Institute)

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

Types of Adaptive Immunity

Active immunity

Protection via introduction of antigen into responsive host, e.g.:

1. Naturally acquired via ___________ or

2. Artificially acquired via ___________

Passive Immunity

Protection via transfer of antibodies or immune cells into a non-immune host, e.g.:

1. Naturally acquired:

2. Artificially acquired: injection of immune serum • Snake bite• Rh+ child with Rh- mother• Treatment of infectious

diseases (??)

Compare to Fig 17.18

Foundation Fig 17.20: Summary of Adaptive Immunity

ImmunologyMicro Flix