Sales force impact on B-to-B brand equity: Conceptual framework and empirical test

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Borrelia burgdorferi Manipulates Innate and Adaptive Immunity to Establish Persistence in Rodent Reservoir Hosts.

Borrelia burgdorferi sensu lato species complex is capable of establishing persistent infections in a wide variety of species, particularly rodents. Infection is asymptomatic or mild in most reservoir host species, indicating successful co-evolution of the pathogen with its natural hosts. However, infected humans and other incidental hosts can develop Lyme disease, a serious inflammatory syndrome characterized by tissue inflammation of joints, heart, muscles, skin, and CNS. Although B. burgdorferi infection induces both innate and adaptive immune responses, they are ultimately ineffective in clearing the infection from reservoir hosts, leading to bacterial persistence. Here, we review some mechanisms by which B. burgdorferi evades the immune system of the rodent host, focusing in particular on the effects of innate immune mechanisms and recent findings suggesting that T-dependent B cell responses are subverted during infection. A better understanding of the mechanisms causing persistence in rodents may help to increase our understanding of the pathogenesis of Lyme disease and ultimately aid in the development of therapies that support effective clearance of the bacterial infection by the host's immune system

Dual role for B-1a cells in immunity to influenza virus infection

B-1 cells are known to contribute most of the “natural antibodies” that are secreted in the steady state, antibodies which are crucial for protection against many pathogens including influenza virus. Whether the CD5+ B-1a subset plays a role during an active immune response is incompletely understood. In contrast to recent data suggesting a passive role for B-1a cells, data provided here show strong highly localized activation of B-1 cells in the draining lymph nodes of the respiratory tract after influenza infection. B-1 cells are identified as a major source for both steady state and infection-induced local virus-neutralizing IgM. The CD5+ B-1a subset is the main B-1 cell subset generating this response. B-1a cell responses are generated by their increased local accumulation rather than by antigen-specific expansion. Our study reveals that during infection with influenza, CD5-expressing B-1a cells respond to and contribute to protection, presumably without the need for B cell receptor–mediated antigen-specific signals, which are known to induce the death of B-1a cells rather than activation. With that, our data reveal fundamental differences in the response regulation of B-1 and B-2 cells during an infection

TLR induces reorganization of the IgM-BCR complex regulating murine B-1 cell responses to infections.

In mice, neonatally-developing, self-reactive B-1 cells generate steady levels of natural antibodies throughout life. B-1 cells can, however, also rapidly respond to infections with increased local antibody production. The mechanisms regulating these two seemingly very distinct functions are poorly understood, but have been linked to expression of CD5, an inhibitor of BCR-signaling. Here we demonstrate that TLR-mediated activation of CD5+ B-1 cells induced the rapid reorganization of the IgM-BCR complex, leading to the eventual loss of CD5 expression, and a concomitant increase in BCR-downstream signaling, both in vitro and in vivo after infections of mice with influenza virus and Salmonella typhimurium. Both, initial CD5 expression and TLR-mediated stimulation, were required for the differentiation of B-1 cells to IgM-producing plasmablasts after infections. Thus, TLR-mediated signals support participation of B-1 cells in immune defense via BCR-complex reorganization