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Review
. 2019 Nov 22:10:2738.
doi: 10.3389/fimmu.2019.02738. eCollection 2019.

Host Immune Responses and Immune Evasion Strategies in African Trypanosomiasis

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Review

Host Immune Responses and Immune Evasion Strategies in African Trypanosomiasis

Chukwunonso Onyilagha et al. Front Immunol. .

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.

Keywords: African trypanosomes; immune evasion; immunity; immunosuppression; resistance; susceptibility.

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Figures

Figure 1
Figure 1
Events preceding immune evasion by parasites. Following infection, trypanosomes are able to undergo antigenic variation, disrupt B cell homeostasis, and initiate polyclonal B cell activation leading to the production of non-specific antibody responses. In addition, the infection is also associated with the induction of suppressor cells like Tregs and MDSCs. These events contribute to immune evasion by the parasites resulting in poor parasite control, increased inflammation, immune exhaustion, disease exacerbation, and death in untreated animals.

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References

    1. Baral TN. Immunobiology of African trypanosomes: need of alternative interventions. J Biomed Biotechnol. (2010) 2010:389153. 10.1155/2010/389153 - DOI - PMC - PubMed
    1. Kristjanson PM, Swallow BM, Rowlands GJ, Kruska RL, de Leeuw PN. Measuring the costs of African animal trypanosomosis, the potential benefits of control and returns to research. Agric Syst. (1999) 59:79–98. 10.1016/S0308-521X(98)00086-9 - DOI
    1. Hursey BS. The programme against African trypanosomiasis: aims, objectives and achievements. Trends Parasitol. (2001) 17:2–3. 10.1016/S1471-4922(00)01851-1 - DOI - PubMed
    1. Kuzoe FA. Current situation of African trypanosomiasis. Acta Trop. (1993) 54:153–62. 10.1016/0001-706X(93)90089-T - DOI - PubMed
    1. Simarro PP, Cecchi G, Paone M, Franco JR, Diarra A, Ruiz JA, et al. . The Atlas of human African trypanosomiasis: a contribution to global mapping of neglected tropical diseases. Int J Health Geogr. (2010) 9:57. 10.1186/1476-072X-9-57 - DOI - PMC - PubMed

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