Biology 102
Fall 2001
R. Brundage
Lecture 2: Part IV
Immunity II: Chapter 40
B.Antigen-Presenting CellsThe Triggers for Immune Responses
1.Located on the membranes of the bodys cells are proteins called MHC
markers.
2.When an antigens enter the body, they are engulfed and destroyed by
macrophages but not completelythe antigen becomes attached to the
MHC marker to form an MHC-antigen complex, which is then displayed
on the macrophages surface.
3.Any cell that displays antigen with a suitable MHC marker is known as an
antigen-presenting cell and will be noticed by lymphocytes.
C.Key Players in Immune Responses
1.Helper T cells: recognize antigen-MHC complexes and respond by
secreting substances that promote the formation of large populations of
effector and memory cells.
2.Cytotoxic T cells: destroy infected (viruses for example)body cells and
tumor cells in what is referred to as cell-mediated immune responses.
3.B cells: and their progeny (effector cells) produce antibodies, which are
specific substances that tag targets for destruction; this is called the
antibody-mediated response.
D.Control of Immune Responses
1.When effector cells have reduced the antigen-bearing agents in the body,
the immune response slows and then stops.
2.Inhibitory signals from cells with repressor roles also help shut down
responses.
I.Lymphocyte Battlegrounds
A.Locations such as tonsils and lymph nodules allow antigen-presenting cells and
lymphocytes to intercept invaders just after they penetrate surface barriers.
B.Before antigen can reach the blood, it must trickle through lymph nodes, which
are packed with defending cells
II.Cell-Mediated Responses
A.T Cell Formation and Activation
1.T lymphocytes arise from stem cells in the bone marrow and then travel to
the thymus gland where the helper T and cytotoxic T cells complete their
development by acquiring T-cell receptors (TCRs).
2.Virgin T cells ignore both unadorned MHC markers and free antigen, but
they do recognize and bind with antigen-MHC complexes on
antigen-presenting cells; this causes them to divide repeatedly to form
clones.
B.Functions of Effector T Cells
1.The effector helper T cells (clones) secrete interleukins, which stimulate
further cell divisions and differentiation.
2.The clones of cytotoxic T cells recognize the antigen-MHC complexes on
infected cells and kill them by punching holes in their cell membranes
with proteins called perforins.
3.The main targets of cell-mediated responses are cells infected with
intracellular pathogens, tumor cells, and cells of organ transplants.
C.Regarding the Natural Killer Cells
1.NK cells appear to be lymphocytes (but not B or T) produced in the bone
marrow.
2.Natural killer (NK) cells kill tumor cells and virus-infected cells
spontaneously, without the presence of antibodies.
III.Antibody-Mediated Responses
A.B Cells and The Targets of Antibodies
1.B cells, like T cells, also arise from stem cells and proceed along a path to
full differentiation which includes the production of proteins called
antibodies.
a.Each antibody has sites that will match up with only one kind of
antigen.
b.Each antibody is Y-shaped with the tail embedded in the B cell
membrane and the two arms (bearing the antigen receptors)
sticking outward.
2.When a "virgin" B cell makes contact with an antigen, it becomes
sensitive to communication signals helper T cells that have been activated
by antigen-presenting cells.
a.In the presence of interleukins (from the helper Ts), B cells
sensitized to the antigen will divide rapidly to produce clone
cells, all making the same antibody which will tag invaders for
destruction by the phagocytic cells.
b.Part of the clone population differentiates into effector cells that
continue to make antibody; other cells become memory cells.
3.The main targets of antibody-mediated responses are extracellular
pathogens and toxins, which remain outside the bodys cells.
B.The Immunoglobulins
1.B cells produce four classes of antibodies known as the
immunoglobulins.
2.All have antigen-binding sites, but each class also has other specialized
functions:
a.IgM, the first to be secreted during immune response, trigger the
complement cascade.
b.IgG antibodies activate complement proteins and neutralize many
toxins; they are long lasting and can cross the placenta to protect
the fetus.
c.IgA, present in saliva, tears, and mucus, helps repel invaders at
the start of the respiratory system.
d.IgE antibodies stimulate basophils and mast cells to secrete
histamine.
IV.Focus on Health: Cancer and Immunotherapy
V.Immune Specificity and Memory
A.Formation of Antigen-Specific Receptors
1.All B cells have the same genes coding for the polypeptides in each arm
of the antibody molecule, but different polypeptides can be made by
shuffling the genes into millions of combinations to produce antibodies
against numerous agents.
2.The clonal selection hypothesis proposes that a lymphocyte activated by a
specific antigen will divide and give rise to a clone of cells that are
specific only to that antigen.
B.Immunological Memory
1."Immunological memory" is the basis of the secondary immune response
to a previously encountered agent.
2.After a primary immune response, some B and T cells continue to
circulate for years as memory cells, which can divide when they meet the
antigen again.
3.The secondary response is more rapid, of greater magnitude, and of
longer duration.
VI.Immunity Enhanced, Misdirected, or Compromised
A.Immunization
1.Active immunization involves a deliberate production of memory cells by
a vaccine that is made from killed or weakened bacteria or viruses.
2.If a person has already been exposed to bacterial pathogens, passive
immunity can be temporarily conferred by injecting antibodies.
B.Allergies
1.An allergy is a secondary immune response to a normally harmless
substance, an allergen such as pollen or certain foods.
2.Exposure triggers production of IgE antibodies, which cause the release
of histamines and prostaglandins.
3.A local inflammatory response results; death can even occur due to
anaphylactic shock, a condition in which air passages leading to the lungs
constrict, fluid escapes too rapidly from capillaries, and blood pressure
drops.
C.Autoimmune Disorders
1.In autoimmune disorders, lymphocytes turn against the bodys own cells.
2.Grave s disorder is an overproduction of thyroid hormones, which
elevate metabolic rates, heart fibrillations, nervousness, and weight loss.
3.In myasthenia gravis, antibodies are directed against acetylcholine
receptors on skeletal muscle cells causing weakness.
4.Rheumatoid arthritis is an inflammation of the joints caused by antibody
that treats the bodys own IgG molecules as if they were antigens.
D.Deficient Immune Responses
1.When cell-mediated immunity is weakened, infections that would
normally not be serious become life-threatening.
2.In acquired immune deficiency syndrome (AIDS), the cause is the human
immunodeficiency virus (HIV).
VII.Focus on Health: AIDSThe Immune System Compromised