In addition to the lack of a shift in the breadth or magnitude of the anti-Msp2 antibody production in response to immunization, targeting of specific CR or HVR epitopes did not correlate with protective immunity. One possible exception was the conserved region epitope P5, which was recognized by four of ten of the immunized animals,

two of which were protected from infection. ABT-737 molecular weight None of the infected animals had antibody to P5. Among the infected animals, the anti-Msp2 antibody response was measured during the control of the initial bacteremic peak. At this time point, high titers to the CR but not the HVR of Msp2 correlated with control of bacteremia. This was not the case in immunized animals in which there was no correlation between the anti-Msp2 antibody response and bacteremia, supporting the hypothesis that separate immunologic mechanisms control bacteremia in infected animals as compared to immunized animals. Among Galunisertib molecular weight the immunized animals,

there was no correlation between the breadth or magnitude of the anti-Msp2 antibody response and protection from infection. Among the animals that developed bacteremia in the face of immunization, there was a trend toward the animals with the highest titers to both the HVR and the CR also having the highest bacteremia. This was particularly true for the response to the HVR peptides I.1, III.1, and III.3. The reason for this is unknown, but helps to

emphasize the point, that while immunized animals were better able to control bacteremia as compared to infected animals, epitopes other than those on Msp2 were likely responsible for that immunologic control. A strong antibody response is known to be directed against Msp2 during acute infection. However, the data presented here fail to show a relationship between antibody to the HVR and control of bacteremia in either immunized or infected animals during acute infection. This was not due to a lack of Msp2 epitopes in the immunogen as immunization resulted in the production of antibody to all possible regions of Msp2, except one, thus we can infer that the immunogen contained Dipeptidyl peptidase a wide variety of the Msp2 epitopes. Additionally, the antibody repertoire did not change significantly in response to infection. Thus, a similar antigenic repertoire was available in the immunogen and during infection. These data suggest that the anti-Msp2 antibody response may be irrelevant during the control of the initial bacteremia, and are consistent with previously reported findings indicating that animals immunized with Msp2 variants were not protected when challenged with A. marginale expressing similar variants as those in the immunogen [16].