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Background .  Plasmodium yoelii  17XNL is a nonlethal malaria strain in mice of different genetic backgrounds including the C57BL/6 mice (I-A b /I-E null ) used in this study as a control strain. We have compared the trends of blood stage infection with the nonlethal murine strain of  P. yoelii  17XNL malaria protozoan in immunocompetent Nonobese Diabetic (NOD) mice prone to type 1 diabetes (T1D) and C57BL/6 mice (control mice) that are not prone to T1D and  self -cure the  P. yoelii  17XNL infection. Prediabetic NOD mice could not mount a protective antibody response to the  P. yoelii  17XNL-infected red blood cells (iRBCs), and they all succumbed shortly after infection. Our data suggest that the lack of anti- P. yoelii  17XNL-iRBCs protective antibodies in NOD mice is a result of parasite-induced, Foxp3 +  T regulatory (Treg) cells able to suppress the parasite-specific antibody secretion.  Conclusions . The NOD mouse model may help in identifying new mechanisms of B-cell evasion by malaria parasites. It may also serve as a more accurate tool for testing antimalaria therapeutics due to the lack of interference with a preexistent  self -curing mechanism present in other mouse strains.

Nonobese Diabetic (NOD) Mice Lack a Protective B-Cell Response against the “Nonlethal”Plasmodium yoelii17XNL Malaria Protozoan