Microbiology and Immunology

WORLD OF MICROBIOLOGY AND IMMUNOLOGY Immunologic therapies

301

•

of the various immunoglobulins. Differences in their structure

outside of the antigen binding region, in an area known as the

constant region, accounts for differences in the immunoglobu-

lin in other functions. These other functions are termed effec-

tor functions, and include features such as the recognition and

binding to regions on other cells, and the stimulation of activ-

ity of an immune molecule known as complement.

The vast diversity of immunoglobulin specificity is due

to the tremendous number of variations that are possible in the

variable region of an immunoglobulin. A certain immune cell

known as a B cell produces each particular immunoglobulin.

Thus, at any particular moment in time, there are a myriad of

B cellsactively producing a myriad of different immunoglob-

ulins, in response to antigenic exposure.

Immunoglobulins can exist in two forms. They can be

fixed to the surface of the B cells that have produced them. Or

they can float freely in body fluids, essentially patrolling until a

recognizable antigen is encountered. The protection of the body

from invading antigens depends on the production of

immunoglobulins of the required type and in sufficient quantity.

Conditions where an individual has a reduced number

of immunoglobulins or none at all of a certain type is known

as an immunoglobulin deficiency syndrome. Such syndromes

are typically the result of damage to B cells.

People with immunoglobulin deficiencies are prone to

more frequent illness than those people whose immune sys-

tems are fully functional. Often the illnesses are caused by

bacteria, in particular bacteria that are able to form a capsule

surrounding them. A capsule is not easily recognized by even

an optimally performing immune system. As well,

immunoglobulin deficiency can render a person more suscep-

tible to some viral infections, in particular those caused by

echovirus, enterovirus, and hepatitisB.

Immunoglobulin deficiencies can take the form of a pri-

mary disorder or a secondary disorder. A secondary deficiency

results from some other ongoing malady or treatment. For

example, chemotherapyfor a cancerous illness can compro-

mise the immune system, leading to an immunodeficiency.

Once the treatment is stopped the immunodeficiency can be

reversed. A primary immunodeficiency is not the result of an

illness or medical treatment. Rather, it is the direct result of a

genetic disorder or a defect to B cells or other immune cells.

X-linked agammaglobulinemia results in an inability of

B cells to mature. This results in the production of fewer B

cells and in a lack of “memory” of an infection. Normally, the

immune system is able to rapidly respond to antigen that has

been encountered before, because of the “memory” of the B

cells. Without this ability, repeated infections caused by the

same agent can result.

Another genetically based immunoglobulin deficiency

is known as selective IgA deficiency. Here, B cells fail to

switch from producing IgM to produce IgA. The limited

amount of IgA makes someone more prone to infections of

mucosal cells. Examples of such infections include those in

the nose, throat, lungs, and intestine.

Genetic abnormalities cause several other immunodefi-

ciency syndromes. A missing stretch of information in the

genethat codes for the heavy chain of IgG results in the pro-

duction of an IgG that is structurally incomplete. The result is

a loss of function of the IgG class of antibodies, as well as the

IgA and IgE classes. On a subtler level, another genetic mal-

function affects the four subclasses of antibodies within the

IgG class. The function of some of the subclasses are affected

more so than other subclasses. Finally, another genetic muta-

tion destroys the ability of B cells to switch from making IgM

to manufacture IgG. The lack of flexibility in the antibody

capability of the immune system adversely affects the ability

of the body to successfully fight infections.

Transient hypogammaglobulinemia is an immunodefi-

ciency syndrome that is not based on a genetic aberration.

Rather, the syndrome occurs in infants and is of short-term in

duration. The T cellsof the immune system do not function

properly. Fewer than normal antibodies are produced, and

those that are made are poor in their recognition of the anti-

genic target. However, as the immune system matures with

age the proper function of the T cells is established. The cause

of the hypogammaglobulinemia is not known.

Immunoglobulin deficiency syndromes are curable only

by a bone marrow transplant, an option exercised in life-

threatening situations. Normally, treatment rather than cure is

the option. Prevention of infection, through the regular use of

antimicrobial drugs and scrupulous oral health are important

to maintain health in individuals with immunoglobulin defi-

ciency syndromes.

See alsoImmunochemistry; Immunodeficiency disease syn-

dromes; Immunodeficiency diseases; Immunodeficiency;

Immunogenetics; Immunologic therapies; Immunological

analysis techniques; Immunology; Immunosuppressant drugs

IImmunologic therapiesMMUNOLOGIC THERAPIES

Immunologic therapy is defined as the use of medicines that

act to enhance the body’s immune response as a means of

treating disease. The drugs can also aid in the recovery of the

body from the harmful effects of immune-compromising treat-

ments like chemotherapyand radiation.

Both microorganism-related infections and other mal-

adies that are due to immune deficiency or cell growth defects

are targets of immunologic therapy.

The emphasis in immunologic therapy is the application

of synthetic compounds that mimic immune substances that

are naturally produced in the body. For example, a compound

called aldesleukin is an artificial form of interkeukin-2, a nat-

ural compound that assists white blood cells in recognizing

and dealing with foreign material. Other examples are filgras-

tim and sargramostim, which are synthetic version of colony

stimulating factors, which stimulate bone marrow to make the

white blood cells, and epoetin, an artificial version of erythro-

poietin, which stimulates the marrow to produce red blood

cells. Thrombopoietin encourages the manufacture of

platelets, which are plate-shaped components of the blood that

are vital in the clotting of blood. As a final example, synthetic

forms of interferon are available and can be administered to

womi_I 5/6/03 3:23 PM Page 301