Essay on how parasites evade the immune system - textbook 9 Sept 2014 Kenneth Bixgorin

First, a parasite may evade by means of where they reside. Ascaris (hookworm) moves to the small
intestine where IgA is secreted but is ineffective. Complement or phagocytosis is not found in the
intestine. Also, Entamoeba histolytica digests the mucosa in the large intestine (overcoming innate
immunity surfaces), causing ulceration and abscess.

Second, a parasite may envelop itself using cystic membranes, as of juvenile cestodes.

Third, a parasite may go undetected by the immune system. Plasmodium antigen in the outer host
membrane are not recognized by cell-mediated effectors. Additionally, indigestible hemozoin is
engulfed by macrophages, weakening phagocytosis.

Fourth, a parasite may use antigen variation. African trypanosomes continually vary antigen, so that
by the time a host antibody recognizes the already changed antigen, it is too late. Also trypanosomes
secrete substances to suppress antibody and cell-mediated responses (via polyclonal B-cell
activation), which produces nonspecific IgG, exhausting the immune system. They also suppress IL2,
IL2R, and T-cells.

Fifth, a parasite may misdirect the immune response. Leishmania invade macrophages near the site
of infection and then move into the RES. A strong humoral response suppresses the later needed
cell-mediated immunity.

Sixth, a parasite may adsorb host antigen so a host sees only self, as in the case of the blood fluke
Schistosoma. Additionally, there is polyclonal lymphocyte activation (as above).

A multiplicity of mechanisms are listed by parasite in tables 3.3 and 3.4:

Schistosoma use Ig-cleaving protease to cleave Ab and glutathione S-transferase against ROIs.
Plasmodium use Ag variation and molecular mimicry, induction of blocking Ab, and altered peptides
to alter memory T-cells.
Trypanosoma brucei use variant-specific surface glycoproteins, alter T & B-cell populations, abnormal
activation of macrophages, production of gp63-like protein to resist complement, and change of CD8
+

T cells cytokines to increase IFN- and decrease IL-2 and IL-2R.
Trypanosoma cruzi alter phagocytosis to affect thymus dependent and independent response,
secretes mucin to bind macrophages, produce blocking IgM affecting inhibitory Ab, and affect
turnover of surface molecules, P-lipases, and complement regulators to resist complement.
Entamoeba histolytica are cytolytic, have proteases that degrade Ab, acquire complement regulating
factor, shed immune complexes by capping and inactivating complement components, release
monocyte locomotion inhibition factor, produces prostaglandin E2 to impair macrophages, and
induces IL-4 and IL-10 to modulate T
H
1 response.
Leishmania inhibit phagolysosomes and proteolytic enzymes in macrophages, abnormally activate
protein kinase C and scavenge ROIs inhibiting respiratory burst, shed membrane attack complexes
resisting lysis, repress MHC2 expression preventing Ag presentation, inhibit production of IL-1, TNF,
IL-12, IL-6, and chemokines suppressing inflammation, interfere with production of transforming
growth factor- and IL-10 resulting in immunosuppression, and interfere with intracellular signaling,
including JAK-STAT downstream from IFN- repressing IFN-inducible genes.