The immune responses evoked by parasites are not unusual and are essentially the same as those involved in immunity to other infectious organisms but what is different is their complexity in response to diverse antigens expressed by different stages of complicated life cycles, often in different situations in the host. This leads to a plethora of antibody-independent and antibody-dependent responses which, over a period of time, can give rise to misdirected immune responses leading to pathological changes instead of protection. For example, during the course of many infections, parasite-derived molecules are deposited on host tissues and elicit autoimmune responses which contribute to the pathology of the infection. Some parasites, such as T. cruzi, evade the immune response by mimicking host molecules and, if effective, this is very successful but, if unsuccessful, can also initiate autoimmune reactions. Typically, parasitic infections are accompanied by periods of immunodepression as the host switches off what is becoming an ineffective or dangerous immune response, rendering the host susceptible to concurrent infections as happens in malaria and African trypanosomiasis. During the course of long, chronic infections various aspects of the cytokine network are activated and the effector molecules produced are not necessarily beneficial. For example, in malaria the production of TNFa is beneficial but in excess is detrimental, and in schistosomiasis potentially protective cytokine-mediated immune responses lead to granulomas around nonthreatening eggs deposited in tissues. For these reasons, current interest in immunity to parasites is being concentrated on an understanding of the overall control of the immune response which is brought about by the interactions of the various cytokines involved in the cytokine network.

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