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The
Human Immune Response System
An
overview of the system
The human
immune response system recognizes pathogens
and acts to remove, immobilize, or neutralize them.
The immune system is antigen-specific (responding to
specific molecules on a pathogen) and has memory (its
defense to a pathogen is encoded for future activation).
The immune system relies on several components to fight
an infecting pathogen. T cells are lymphocytes that
circulate between the blood, lymph, and lymphoid organs
to trigger a systemic immune response with antigen-receptors
on the T cell membrane. B cells are lymphocytes that
activate the primary immune response when antigens bind
to their receptors, causing the B cells to proliferate.
Daughter cells of B cells later differentiate into antibody-releasing
plasma cells. B cells also comprise the immune system's
memory (see
diagram).
Antibodies,
also called immunoglobulins, are divided into five classes
by structure and function, enabling them to recognize
a wide spectrum of antigens. Antibody functions include
complement fixation that can lead to antigen-cell lysis
(rupture) and can cause inflammation. Antibodies also
generate a neutralization response where viruses and
bacteria are destroyed by phagocytes. Agglutination,
or clumping together, of foreign cells are caused by
B cells' promotion of complex cross-linking of antibodies
binding to antigens. These agglutinated cells are phagocytized.
B cells are cloned in massive quantities for a single
specific antigen.
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Immune
response to T. cruzi
The
human immune response to T. cruzi infection is
inadequate; it provides only a partial defense at best.
The immune system's response at its worst causes the
defense mechanisms to turn on the body it is intended
to protect, thus often causing more harm to the person
than does T. cruzi.  As
T. cruzi immunizes humans to their own antigens,
human antibodies attack myocardial and neural cells.
Complement
in humans does not become activated solely by T.
cruzi invasion; antibodies must be present for complement
to bind to a specific T. cruzi antigen. This
allows T. cruzi to have time to infect human
tissue. Parasite strain and an individual's immune competence
are prime factors in determining the T. cruzi's
pathology of an individual.
Once infected
with T. cruzi, humans acquire partial immunity
or resistance to the severe pathologies of Chagas' disease's
acute phase through subsequent infections of T. cruzi.
This guards many individuals who live in highly endemic
areas from the acute symptoms of chagas. Complete removable
of the parasite from these individuals would risk the
onset of acute chagas through future infection, which
is deadly - especially for children.
T.
cruzi incorporates certain host cell membrane
proteins onto its surface thereby masking its antigenic
signal to the immune system's lymphocytes. T. cruzi
can also cleave antibody molecules on its surface thereby
escaping the immune response's detection. T. cruzi
frequently invade monocytes, a circulating phagocyte.
Intracellular phagocytosis bring amastigotic T. cruzi
into tissue cells where they can proliferate. Once inside
tissue cells, T. cruzi are undetected by immune
response. Trypomastigotes remain in the blood stream
for a short period of time so that the T. cruzi-specific
immunoglobulins don't have sufficient time to be activated.
T. cruzi employs successful strategies to escape
the remarkably potent immune response system. By masking
themselves or by eluding the response mechanisms, the
parasite is able to adapt to survive and continue the
life of the species.
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Immune
response that damages the human body
Unintentional
damage is done to the body's
otherwise healthy tissue as the response system attacks
what it recognizes as a trigger for a defensive response
but does not recognize that it is attacking itself.
This is what's known as an autoimmune reaction.  Autoimmune
responses are responsible in large part for the destructive
symptoms of Chagas disease. This pathology is referred
to as immunopathology. Severe inflammation occurs around
tissue that embody amastigotes as the amastigotes release
themselves from the tissue's dead cells. Among the tissue
most often encysted is myocardial neural plexes. Plexes
are networks of nerves that serve a variety of organs
and functions. Digestive system neural plexes are targets
as well, namely in the colon and esophagus. During the
acute phase of chagas, B and T cells are incited to
produce antibodies. Since T. cruzi is able to
mask its presence in the blood, these antibodies do
not attack T. cruzi but instead go after cell
membrane antigenic components called epitopes, that
the body's healthy cells and T. cruzi share.
Research is being done to isolate the epitope and how
T. cruzi uses it to elude recognition by the
immune system.
Scientists
work to find a cure to T. cruzi's infecting the
human species. As research continues into how T.
cruzi uses the human body as a host, the disciplines
of parasitology and immunology learn much about how
these organisms adapt and thrive in changing environments.
T. cruzi proves to be a formidable opponent in
the fight.
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