Host Immune Responses and Immune Evasion Strategies in African Trypanosomiasis

Abstract

Parasites, including African trypanosomes, utilize several immune evasion strategies to ensure their survival and completion of their life cycles within their hosts. The defense factors activated by the host to resolve inflammation and restore homeostasis during active infection could be exploited and/or manipulated by the parasites in an attempt to ensure their survival and propagation. This often results in the parasites evading the host immune responses as well as the host sustaining some self-inflicted collateral tissue damage. During infection with African trypanosomes, both effector and suppressor cells are activated and the balance between these opposing arms of immunity determines susceptibility or resistance of infected host to the parasites. Immune evasion by the parasites could be directly related to parasite factors, (e.g., antigenic variation), or indirectly through the induction of suppressor cells following infection. Several cell types, including suppressive macrophages, myeloid-derived suppressor cells (MDSCs), and regulatory T cells have been shown to contribute to immunosuppression in African trypanosomiasis. In this review, we discuss the key factors that contribute to immunity and immunosuppression during T. congolense infection, and how these factors could aid immune evasion by African trypanosomes. Understanding the regulatory mechanisms that influence resistance and/or susceptibility during African trypanosomiasis could be beneficial in designing effective vaccination and therapeutic strategies against the disease.

Organotypic endothelial adhesion molecules are key for Trypanosoma brucei tropism and virulence

“…However, the cellular and molecular adaptations that allow parasite tropism are still poorly understood. For many parasites, tropism to specific organs is an essential step of their life cycle, because the organs provide a niche for persistence, latency or dormancy, massive replication and/or growth, protection from the host immune responses, or differentiation into alternative stages essential for completion of the life cycle, among others ( Boyett and Hsieh, 2014 ; Fernandes and Andrews, 2012 ; Guérin and Striepen, 2020 ; Lima and Lodoen, 2019 ; Onyilagha and Uzonna, 2019 ; Prudêncio et al., 2006 ; Rénia and Goh, 2016 ; Silva Pereira et al., 2019 ; Venugopal et al., 2020 ).…”

African Trypanosomosis Permanently Obliterates DTPa Vaccine Induced Memory so That Post-treatment Bordetella Pertussis Challenge Fails to Trigger a Protective Recall Response

“…In an experimental setting, we have previously shown that the human DTPa vaccine loses efficacy during active T. b. brucei infection. This observation could be explained by the multiple levels of immune suppression that are induced during active trypanosomosis [53][54][55][56]. In contrast, the study here provides data showing that the problem at hand is the active destruction of the functional host immune memory compartment.…”

A Wandering Missionary’s Burden: Persistent Fever and Progressive Somnolence in a Returning Traveler

“…Examination of bone marrow is of low yield in detecting trypanosomes [ 6 ], and bone marrow smear as a means of diagnosis is rare [ 9 , 10 ]. Polyclonal activation of B cells is a hallmark of HAT, resulting in elevated IgG and IgM levels, as well as false-positive antibodies for pathogens, and autoantibodies [ 11 ].…”