Infection with Mycobacterium species induces the formation of granulomas — organised structures of macrophages and lymphocytes that contain, but do not clear, the pathogen. Previous imaging studies by this group showed that granulomas that form in the liver ∼2 weeks after infection with M. bovis bacillus Calmette–Guérin (BCG) contain static macrophages and motile T cells. Additional imaging studies have shown that, following antigen encounter, T cells undergo migrational arrest and form long-lived interactions with antigen-presenting cells in secondary lymphoid organs.
So, to understand the behaviour of effector CD4+ T cells in mycobacterial granulomas, the authors visualised the migration of mycobacterial-antigen-specific (p25) and -nonspecific (OT-II) T cells to and within hepatic granulomas. Similar numbers of activated p25 and OT-II T cells were recruited into the granulomas, indicating that effector T cell accumulation in the granulomas is antigen independent. A comparison of the mean velocity and arrest coefficient of p25 and OT-II T cells within the granulomas in the steady state showed that p25 T cells were only slightly less mobile than OT-II T cells. However, injection of the infected mice with the cognate peptide antigens for p25 and OT-II T cells resulted in almost complete migrational arrest. This indicates that effector T cells are capable of arresting in vivo but that insufficient signals are present in granulomas in the steady state to induce such migrational arrest.
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