Antibodies, produced by B cells, are one of the two main arms of adaptive immunity. Antibodies contribute to the immune response against bacterial pathogens by (1) neutralization of bacteria and their toxins, (2) opsonization of bacteria which promotes uptake by phagocytic cells, and (3) complement activation which enhances opsonization. Humoral responses against many bacterial pathogens are sufficient for protection against disease. For example, vaccines to bacteria such as Bordetella pertussis, the causative agent of whopping cough, or Clostridium tetani, which is responsible for tetanus, induce high titers of antibodies and have high efficacies. Unlike these extracellular bacterial pathogens, the intracellular life cycle of L. monocytogenes allows it to evade this antibody-mediated protection.
Due to the intracellular nature of L. monocytogenes infection, little antibody response is induced during primary L. monocytogenes infection. Although some extracellular bacteria can be found during infection, B cells have little opportunity to encounter L. monocytogenes or its antigen. The low amounts of antibodies that are induced by infection are completely unable to confer protection during a rechallenge infection with L. monocytogenes (Mackaness 1962). Since the majority of the bacteria remain intracellular during infection and spread intercel-lularly without encountering the extracellular milieu, L. monocytogenes-specific antibodies are of limited to no use in controlling bacterial spread.
However, under certain experimental conditions antibodies can affect the course of infection. Although infection itself does not generate high titers of antibodies that are protective, a monoclonal antibody against the pore-forming virulence factor LLO can provide protection by acting intracellularly to neutralize LLO activity (Edelson et al. 1999, Edelson and Unanue 2001). This antibody treatment blocks bacterial escape from the phagosome in macrophages in vitro and in vivo that results in lower bacterial loads. Also, using B cell-deficient mice, natural antibodies in naive animals may play a role in reducing early dissemination of L. monocytogenes into vital organs (Ochsenbein et al. 1999). By trapping bacteria and their antigens in secondary lymphoid organs where specific immune responses are initiated, B cells and antibodies can facilitate the generation of the protective T cell response. Lastly, B cells have been shown to be important in the maintenance of memory CD8 T cells generated during L. monocytogenes infection (Shen et al. 2003). Thus, B cells and antibodies do play a minor, yet significant, role during L. monocytogenes infection by aiding other aspects of the immune response. However, due to the intracel-lular niche of L. monocytogenes, B cells have little impact on the control of infection.
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