Abstract
Trypanosoma vivax is the main species involved in trypanosomosis, but very little is known about the immunobiology of the infective process caused by this parasite. Recently we undertook to further characterize the main parasitological, haematological and pathological characteristics of mouse models of T. vivax infection and noted severe anemia and thrombocytopenia coincident with rising parasitemia. To gain more insight into the organism's immunobiology, we studied lymphocyte populations in central (bone marrow) and peripherical (spleen and blood) tissues following mouse infection with T. vivax and showed that the immune system apparatus is affected both quantitatively and qualitatively. More precisely, after an initial increase that primarily involves CD4+ T cells and macrophages, the number of splenic B cells decreases in a step-wise manner. Our results show that while infection triggers the activation and proliferation of Hematopoietic Stem Cells, Granulocyte-Monocyte, Common Myeloid and Megacaryocyte Erythrocyte progenitors decrease in number in the course of the infection. An in-depth analysis of B-cell progenitors also indicated that maturation of pro-B into pre-B precursors seems to be compromised. This interferes with the mature B cell dynamics and renewal in the periphery. Altogether, our results show that T. vivax induces profound immunological alterations in myeloid and lymphoid progenitors which may prevent adequate control of T. vivax trypanosomosis.
Highlights
African trypanosomes are extracellular parasites that cause sleeping sickness in humans and Nagana in animals
Trypanosoma vivax is responsible for animal trypanosomosis, or Nagana, in cattle and small ruminants
The outbred mouse model infected with a well studied West African T. vivax isolate reproduces the main characteristics of the infection and pathology observed in livestock
Summary
African trypanosomes are extracellular parasites that cause sleeping sickness in humans and Nagana in animals. The involvement of VSGs in protecting the parasites against host specific immunoresponses provided until recently one of the most exquisite models for the study of antigenic variation It followed, for many years, that our understanding of the interaction between African trypanosomes and the immune system was limited to this ‘‘parasite-driven’’ view where the host’s immune response was restricted to the production of specific Abs against VSGs. Whereas anti-VSG Ab doubtless contribute to early control of the infection, resistance to late phases is dependent on specific (parasite-directed) immunoglobulins and seems to rely on T-independent processes since athymic mice and complement-deficient mice infected with T. rhodesiense are able to mount anti parasitic responses that are sufficient to increase mouse survival and healing after an infectious challenge [7,20]
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