Chapter 17.

Adaptive Immunity
and Immunization
Types of Acquired Immunity
• Actively acquired adaptive immunity: the use of antibodies produced by one's
own body
o Naturally acquired: by having disease or infection
o Passively acquired: by receiving vaccine
• Passively acquired adaptive immunity: the use of ready-made antibodies
o Naturally acquired: infants receiving maternal antibodies across placenta
or in milk
o Passively acquired: by receiving injection of gamma globulin or immune
serum

Antigen
• Antigen: biological macromolecules able to elicit immune responses, usually
surface proteins of parasites.
• Epitopes: antigenic determinants. These are surface-exposed, small (3-5 amino
acids) areas of a protein molecule. A single antigen molecule have multiple
epitopes.
• Hapten: a small molecule that converts a normal protein into an antigen. Neither
the molecule itself nor the protein alone is an antigen. Example: penicillin, which
in some individuals binds to proteins molecules and elicit hypersensitivity
("allergy").

General Properties of Adaptive Immunity

• Dual Nature
o Humoral immunity: carried out by antibodies in the blood; most effective
against extracellular parasites (e.g., toxins, bacteria, viruses before
entering the host cell)
o Cell-mediated immunity: carried out by T cells; most effective against
intracellular infection (e.g., virus-infected cells)
• Recognition of self versus nonself
o Destroying foreign substances
o Tolerance of self tissues
o Mechanisms
 Clonal selection: selective propagation of lymphocytes (B or T
cells) that have receptors for a foreign antigen
  Clonal deletion: selective inactivation of lymphocytes that have
receptors for self antigens.
• Specificity: adaptive defenses are specific to pathogen species and strains
• Heterogeneity/Diversity: adaptive immunity is able to defend a great variety of
antigens
• Memory: the ability to respond quickly to previously encountered infections

Humoral Immunity
• Antibodies/Immunoglobins/Ig
o Y-shaped molecules consisting of 2 light chains and 2 heavy chains
o Chains are linked by disulfide fonds and have constant and variable
regions
o Variable regions of light and high chains have antigen-binding sites
o Constant regions have tissue-binding sites that can activate complement,
participate in allergic reactions, and bind to macrophage
• Classes of antibodies
o IgG: main Ig in serum; able to cross placenta; provide long-term immunity
o IgA: mostly in mucus and attached to the digestive, respiratory, and
genitourinary systems
o IgM: pentamer; antibody produced first (in T-independent primary
response)
o IgE: binds to basophils and mast cells, resulting in allergic reaction
o IgD: attached to B cells (not secreted)
• Primary and secondary responses
o Primary response:
 1st exposure to an antigen; long lag period (~5 days); IgM->IgG
switch; memory cells formed
 Two mechanisms: T-dependent (requiring activation by T-helper
cells, causing IgM->IgG switch) and T-dependent (requiring no
activation by T cells; producing IgM; no memory cells produced)
o Secondary response: subsequent exposures; rapid increase and sustained
production of IgG
• Consequences of antigen-antibody reactions: agglutination (sticking together of
microbes), opsonization, activation of complement, cell lysis, and neutralization
(inactivation of toxin, virus particles by the formation of antigen-antibody
complexes)
• Monoclonal antibodies (Mabs): single-type antibodies produced in vitro by a
clone of cultured cells. Mab-producting cells are made by fusion of mouse
myeloma cells (cancerous immune cells) and B cells.

Cell-Mediated Immunity
 • Defense reactions through direct cell-cell contact (unlike molecular-level antigen-
antibody reactions in humoral immunity) between T cells and diseased cells
(virus-infected and cancer cells)
• Activation: stem cells -> T cells -> effector cells (antigen-activated T cells, reside
in thymus gland)
• Activation of helper T cells by MHC-II (Major Histocompetibility Complex,
Class II)
1. Antigen-presenting cells (APCs: B cells, dentritic cells, and macrophages)
ingest antigen and display antigen fragments (combined with MHC, self
molecules) on cell surface
2. MHC-Antigen complex binds to CD4, stimulating clonal proliferation of
the Ag-specific CD4 cells
3. CD4 cells activate cytotoxic T cells (release of destructive enzymes to kill
infected cells), B cells (producing antibodies) and macrophages
(phagocytosis)
• Activation of cytoxic T cells by MHC-I: antigen presenting by infected or cancer
cells (not by APCs)

Immunization
• Active immunization/Vaccination (protection by one's own antibodies; not for
treatment because there is a lag period for antibody production). Types of
vaccines:
o Living, attanuated pathogens (e.g., measles & mumps)
o Dead pathogens (e.g., Rabies)
o Subcellular structures (e.g., recombinant HBV surface antigen)
o Toxoids (denatured toxins, e.g, anthrax, tetanus)
• Passive Immunization (the use of ready-made antibodies; offers immediate but
temporary protection)
o Antisera: contains antibodies against e.g., hepatitis A
o Antitoxins: for treatment of tetanus, snake/spider bites
o Anti-Rh: antibodies given to mother to protect Rh-positive new borns