Helminthic mechanisms of immune evasion

Schistosomes are known to survive intravascularly for many years despite the continuing antiparasite immune response by the infected host. The living schistosomes are capable to reduce surface antigenicity and develop a tegument resistant to immune damage. In addition to this 'camouflage-behavior', these parasites influence cellular immune response using "chemical defenses":

Epidermal Langerhans cells (LCs) are a specific kind of antigen presenting cells and play a key role in immune defense mechanisms and in numerous immunological disorders. Studies have shown that percutaneous infection of mice with the helminth parasite Schistosoma mansoni leads to the activation of LCs but also to their retention in the epidermis. Moreover parasites transiently impair the departure of LCs from the epidermis and their subsequent accumulation as dendritic cells in the draining lymph nodes. The inhibitory effect is mediated by soluble lipophilic factors released by the parasites and not by host-derived antiinflammatory cytokines, such as interleukin-10.

References:

• Pearce, E. J., and A. Sher. 1987. Mechanisms of immune evasion in schistosomiasis. Contrib. Microbiol. Immunol. 8:219-232
• Angeli, V., C. Faveeuw, O. Roye, J. Fontaine, E. Teissier, A. Capron, I. Wolowczuk M. Capron, and F. Trottein F. 2001. Role of the parasite-derived prostaglandin D2 in the inhibition of epidermal Langerhans cell migration during schistosomiasis infection. J. Exp. Med. 193:1135-1147.