Parasites have evolved
sophisticated mechanisms to evade effective host
immune response (see
Table 2. Some
mechanisms of parasite immune evasion.
(1) Seclusion from Immune
promastigotes activate complement and
become taken up by macrophages. Normally, this
would trigger respiratory burst in macrophages;
however, the promastigotes fuse with the cell's
lysosome and produce antioxidants and enzyme
inhibitors to neutralize the effects of the
toxins generated by the macrophage. Moreover,
the larval stage of the muscle nematode
trichinella transforms the muscle cell into
a specialized nurse cell that protects it and
provides nutrients. This parasitic worm survives
there for the lifetime of the host.
(2) Parasites Produce
Activation of leukocytes
produce hydrogen peroxide (H2O2),
superoxide ions, and hydroxy radicals (OH-)
which are toxic to parasites. Parasites have
their own oxygen-scavenging enzymes to protect
themselves from host attack. These include the
enzymes: superoxide dismutase, catalase, and
glutathione peroxidase. All helminth and
protozoan parasites examined to date have at
least on of these enzymes.
(3) Interfering with
completely covered with lipophosphoglycan.
This elongated LPG binds complement, assisting
direct entry of the parasite into macrophages.
The parasite avoids damage by complement by the
extreme length of the LPG. The lytic C5b-9
complex forms too far away from the parasite
(4) Antigenic Variation:
coats itself with a dense protein that comprises
of a single antigen called variant surface
glucoprotein (VSG). The amount of parasites
eventually declines when the host antibodies
recognize this VSG (Figure 6). However,
parasites that have replicated have new VSG, so
the old immune response is no longer effective.
Antigenic variation in African trypanosomes. The
photo is a blood smear showing a trypanosome. Click
The following is a list of
parasites that have been profiled: