Abstract
ABSTRACTDetermining the effector populations involved in humoral protection against genital chlamydia infection is crucial to development of an effective chlamydial vaccine. Antibody has been implicated in protection studies in multiple animal models, and we previously showed that the passive transfer of immune serum alone does not confer immunity in the mouse. Using the Chlamydia muridarum model of genital infection, we demonstrate a protective role for both Chlamydia-specific immunoglobulin G (IgG) and polymorphonuclear neutrophils and show the importance of an antibody/effector cell interaction in mediating humoral immunity. While neutrophils were found to contribute significantly to antibody-mediated protection in vivo, natural killer (NK) cells were dispensable for protective immunity. Furthermore, gamma interferon (IFN-γ)-stimulated primary peritoneal neutrophils (PPNs) killed chlamydiae in vitro in an antibody-dependent manner. The results from this study support the view that an IFN-γ-activated effector cell population cooperates with antibody to protect against genital chlamydia and establish neutrophils as a key effector cell in this response.
Highlights
Determining the effector populations involved in humoral protection against genital chlamydia infection is crucial to development of an effective chlamydial vaccine
Antibody-deficient mice depleted of CD4ϩ T cells are incapable of resolving secondary infection naturally because they are deficient in both protective arms of antichlamydial immunity [9, 11,12,13]
Consistent with the lack of direct neutralizing ability of antibody in vivo [13], these data indicate that immunoglobulin G (IgG), rather than IgM or IgA, conferred protective immunity and that the Fc region of Chlamydia-specific Ig was required for antibody-mediated protection
Summary
Determining the effector populations involved in humoral protection against genital chlamydia infection is crucial to development of an effective chlamydial vaccine. Using the Chlamydia muridarum model of genital infection, we demonstrate a protective role for both Chlamydia-specific immunoglobulin G (IgG) and polymorphonuclear neutrophils and show the importance of an antibody/effector cell interaction in mediating humoral immunity. The results from this study support the view that an IFN-␥-activated effector cell population cooperates with antibody to protect against genital chlamydia and establish neutrophils as a key effector cell in this response. The pathogen will be shuttled along the endocytic/lysosomal pathway, leading to its degradation Support for this mechanism of protection includes antibodymediated protection’s requirement for gamma interferon (IFN-␥) [17], which upregulates expression of FcRs and enhances microbial killing in phagocytes [18, 19]
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