The role of B cells in an early immune response to Mycobacterium bovis
Language English Country Great Britain, England Media print-electronic
Document type Journal Article
PubMed
31862393
DOI
10.1016/j.micpath.2019.103937
PII: S0882-4010(19)31309-9
Knihovny.cz E-resources
- Keywords
- Activating markers, B cells, Cytokines, M. bovis BCG, Receptors,
- MeSH
- B-Lymphocytes * immunology microbiology MeSH
- BCG Vaccine MeSH
- Cytokines metabolism MeSH
- Humans MeSH
- Mycobacterium bovis immunology MeSH
- Mice MeSH
- Primary Cell Culture MeSH
- Immunity, Innate MeSH
- Tuberculosis immunology microbiology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- BCG Vaccine MeSH
- Cytokines MeSH
Mycobacterium tuberculosis is the main etiological agent of tuberculosis. The Bacillus Calmette-Guérin (BCG) microbes that are primarily used as a vaccine against tuberculosis also constitute the dominant infection model for studying the interaction of mycobacteria with the host cell types. The majority of interaction experiments have been conducted using macrophages and monocytes as prototype phagocyte cell types. Here, we report that M. bovis BCG infects mouse primary B cells as well as human B cell line. The complement receptors, along with B cell receptors, are engaged in the process of bacterial entry into the host B cells. Once inside the B cells, the intracellular trafficking of BCG follows the complete endocytic pathway of the ingested particles, which is in contrast to the events taking place during ingestion of BCG by macrophages. In vivo infection of mice with M. bovis BCG activated peritoneal as well as splenic B cells to produce proinflammatory cytokines. This paper further supports the evidence that B cells are involved in a host's early interactions with intracellular bacterial pathogens and participate in the induction of innate defense responses.
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