Trypanosomosis is a chronic parasitic infection, affecting both humans and livestock. A common hallmark of experimental murine infections is the occurrence of inflammation and the associated remodelling of the spleen compartment. The latter involves the depletion of several lymphocyte populations, the induction of T‐cell‐mediated immune suppression, and the activation of monocyte/macrophage cell populations. Here, we show that in experimental T b brucei infections in mice, these changes are accompanied by the alteration of the spleen neutrophil compartment. Indeed, mature neutrophils are rapidly recruited to the spleen, and cell numbers remain elevated during the entire infection. Following the second peak of parasitemia, the neutrophil cell influx coincides with the rapid reduction of splenic marginal zone (MZ)B and follicular (Fo)B cells, as well as CD8+ T and NK1.1+ cells, the latter encompassing both natural killer (NK) and natural killer T (NKT) cells. This report is the first to show a comprehensive overview of all alterations in spleen cell populations, measured with short intervals throughout the entire course of an experimental T b brucei infection. These data provide new insights into the dynamic interlinked changes in spleen cell numbers associated with trypanosomosis‐associated immunopathology.

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Background Trypanosoma brucei brucei (T. b. brucei) evades host immune responses by multiple means, including the disruption of B cell homeostasis. This hampers anti-trypanosome vaccine development. As the cellular mechanism underlying this pathology has never been addressed, our study focuses on the fate of memory B cells (MBCs) in vaccinated mice upon trypanosome challenge. Methods A trypanosome variant surface glycoprotein (VSG) and fluorescent phycoerythrin (PE) were used as immunization antigens. Functional and cellular characteristics of antigen-specific MBCs were studied after homologous and heterologous parasite challenge. Results Immunization with AnTat 1.1 VSG triggers a specific antibody response and isotype-switched CD73 +CD273 +CD80 + MBCs, delivering 90% sterile protection against a homologous parasite challenge. As expected, AnTat 1.1 VSG immunization does not protect against infection with heterologous VSG-switched parasites. After successful curative drug treatment, mice were shown to have completely lost their previously induced protective immunity against the homologous parasites, coinciding with the loss of vaccine-induced MBCs. A PE immunization approach confirmed that trypanosome infections cause the general loss of antigen-specific splenic and bone marrow MBCs, and a reduction in antigen-specific IgGs. Conclusion Trypanosomosis induces general immunological memory loss. This benefits the parasites by reducing the stringency for antigenic variation requirements.