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Updated: Jan 19, 2026

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Experimental malaria in the CBA/N mouse.

A N Jayawardena, C A Janeway, J D Kemp

    Journal of Immunology (Baltimore, Md. : 1950)
    |December 1, 1979
    PubMed
    Summary
    This summary is machine-generated.

    Mice with an X-linked immune defect show reduced resistance to primary malaria infections, linked to a deficient IgM antibody response. However, they develop resistance to reinfection, suggesting distinct immune mechanisms are involved.

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    Area of Science:

    • Immunology
    • Infectious Diseases
    • Genetics

    Background:

    • CBA/N mice possess an X-linked recessive gene causing a B cell defect.
    • This defect impairs responses to thymus-independent antigens.
    • The X-linked immune defect affects B cell subset development.

    Purpose of the Study:

    • To investigate the immune response of CBA/N mice to Plasmodium yoelii malaria.
    • To understand the role of B cell subsets in malaria resistance.
    • To elucidate mechanisms of protective immunity against malaria.

    Main Methods:

    • Comparative study of CBA/N mice and normal controls during primary Plasmodium yoelii infection.
    • Assessment of antibody responses, particularly IgM.
    • Evaluation of resistance transfer using B cells from defective and normal mice.

    Main Results:

    • CBA/N mice experienced more severe and prolonged primary malaria infections.
    • A significant deficiency in IgM antibody response was observed in defective mice.
    • Despite primary infection susceptibility, defective mice developed resistance to reinfection.
    • B cells from CBA/N mice transferred less immunity to naive recipients than those from normal mice.

    Conclusions:

    • Thymus-dependent antibody responses, particularly IgM, are crucial for controlling acute Plasmodium yoelii infections.
    • Resistance to malaria reinfection may involve alternative, thymus-dependent mechanisms.
    • Distinct immunological pathways contribute to malaria protection.