- Basic Concepts in Immunology-
I. Immunology -
The study of the body's defense against pathogens (viruses, bacteria, fungi, parasites)
II. History
and Overview
A. Edward
Jenner (late 1700's) - first vaccination against smallpox:
-
1. Vaccine
- a dead or weakened pathogen used to induce immunity without causing any
disease - worldwide smallpox vaccinations eliminated disease in 1979.
C. Innate
Immunity - present from birth -
fast but nonspecific
-
1. Macrophages - phagocytic cells discovered by Elie Metchnikoff (late 1880's) that can
kill pathogens.
-
1. Antibodies
(Ab) (Immunoglobulins - Ig) - (late 1800's) - substances in serum of infected
individuals that bind pathogen
2. Antigens - substances that bind to antibodies (old definition)
3. Complement (late 1800's) - substances in the serum that destroy pathogens when combined with antibodies
4. Lymphocytes - (1960's) - required for all forms of adaptive immunity - each lymphocyte is specific for certain antigen (monospecificity). All lymphocytes specific to a particular antigen are called a clone
5. Clonal Selection Theory - (1950's) - explains how adaptive immunity works - specific lymphocyte clones exist in small numbers before exposure to pathogen - after exposure, clones specific to pathogen proliferate, increase in number and differentiate into effector cells, such as those that secrete pathogen-specific antibodies
III. Features of Adaptive Immunity
-
A. Clonal
Selection and Tolerance
-
1. Receptor
repertoire
- the receptors on all lymphocytes - recognize all
antigens except self-antigens
2. Tolerance - why we normally don't respond to antigens of our self-antigens - lymphocytes with receptors for self antigens are eliminated early in development (central tolerance)
3. Immunological
memory - when the body re-exposed to pathogen, the adaptive
immunity is faster and stronger because of the increased number of pathogen-specific
lymphocytes
-
1. B
cells and T cells - B-cells secrete antibody (as plasma cells);
T-cells develop into effector cells that either kill pathogen- infected
cells or activate other parts of the immune system
2. Where
are lymphocytes found?
-
a. Central
Lymphoid Organs - Bone Marrow and Thymus
b. Peripheral Lymphoid Organs - Lymph Nodes (LN), Spleen (Spl)
c. Mucosal Surfaces - e,g, Gut-Associated Lymphoid Tissues (GALT) - tonsils, peyers patches of small intestine
d. In
Circulation - Blood and Lymph
4. How do lymphocytes make such a large repertoire of receptors? They rearrange gene segments during differentiation - once rearranged to make a specific type of receptor, the change is permanent, and all the progeny of those cells will have the same receptor. Many types of receptors can be made in this way - called 'combinatorial diversity'
5. What is the antigen receptor on B-cells and T-cells? membrane-bound Ig on B-cells, T-cell receptor on T-cells
6. How
are self-reactive lymphocytes eliminated during development?
-
a. Tolerance
- cells that respond to self-Ag are killed in a process called 'clonal
deletion'
-
1. Where
in the body do lymphocytes encounter antigen? - in the peripheral
(secondary) lymphoid organs - LN or spleen
2. How does antigen get from site of infection? - via blood or lymph - lymphocytes recognize antigens and become effector cells
3. Filter of the lymph - Lymph nodes
4. Filter of the blood - Spleen
5. Characteristics common to Spleen, LN and GALT - There are distinct areas for B cells and T cells - B cells that differentiate into antibody-secreting cells are in germinal centers near the boundary of B and T cell areas
6. Activated lymphocytes - differentiate into effector cells - cell proliferation causes clonal expansion (formation of lymphoblasts) followed by differentiation into effectors - clonal expansion is characteristic of adaptive immunity
7. Co-stimulatory
signals required for activation of lymphocytes
-
a. B
cells - 1st signal is binding of Ag to surface Ig; second signal
provided by T cells (soluble factors called "cytokines")
b. T cells - Ist signal is binding of Ag to T cell receptor (TCR); second signal provided by antigen-presenting cells (APC), which are B-cells, macrophages, or dendritic cells APC trap antigens and present them to T cells
IV. Immune response to pathogens
-
A. Humoral
Immunity - mediated by Ig - good against extracellular pathogens
and toxins (e.g., from bacteria). Antibodies can function in 3 ways:
-
1. Neutralization
- physical binding by Ab
2. Opsonization - binding of Ab to bacteria causes it to be ingested more rapidly by macrophages
3. Activation
of complement
- can lyse and kill bacteria
-
1. Cytotoxic
T cells - can destroy cells infected with viruses
2. Helper T-cells - activate other cells of immune system
3. Macrophages - can be activated by T cells and then kill intracellular pathogens
V. Major Histocompatibility Complex (MHC) Antigens
-
A. T
cells recognize antigen bound to MHC molecules
B. MHC Class I bearing cells (most body cells) - interact with CD8 positive 'cytotoxic' T-cells that act by direct cell killing
C. MHC Class II bearing cells (antigen presenting cells) - interacts with CD4 positive 'helper' T-cells, which activate other T cell and B cell responses
VI. Innate Immunity -
operates during early stages of infection - this immunity is induced, but is nonspecific
-
A.
Complement - can kill some bacteria even in absence of Ab
B. Acute Phase Proteins - made by liver - can also kill some bacteria
C. Macrophages - can phagocytose bacteria in absence of Ab
D. Neutrophils and others
VII. Immune system in health and disease
-
A. 'Good'
immunity - resistance against second infections - ability to
be immunized - possible cancer treatment
B. 'Bad' immunity - transplant rejections allergies (immunodeficiency (including AIDS), and autoimmune disease
By Dr. J.A.Wise Dept of Biology, Hampton University