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T Cells Following Intranasal Infection with Mycobacterium bovis Bacillus Calmette-Guérin1
* Department of Biopathology, University of Palermo, Palermo, Italy;
King’s College London at Guy’s Dental and Medical School, London, United Kingdom;
Center for Applied Microbiology and Research, Salisbury, United Kingdom; and
Institute of Advanced Diagnostic Methodologies, National Research Council, Palermo, Italy
The lungs are considered to have an impaired capacity to contain
infection by pathogenic mycobacteria, even in the presence of effective
systemic immunity. In an attempt to understand the underlying cellular
mechanisms, we characterized the 
T cell population following
intranasal infection with Mycobacterium bovis bacillus
Calmette-Guérin (BCG). The peak of T cell expansion at 7
days postinfection preceded the 30 day peak of 
T cell expansion
and bacterial count. The expanded population of T cells in the
lungs of BCG-infected mice represents an expansion of the resident
V2 T cell subset as well as an influx of V1 and of four different
V gene-bearing T cell subsets. The T cells in the lungs of
BCG-infected mice secreted IFN- following in vitro stimulation with
ionomycin and PMA and were cytotoxic against BCG-infected peritoneal
macrophages as well as against the uninfected J774 macrophage cell
line. The cytotoxicity was selectively blocked by anti- TCR
mAb and strontium ions, suggesting a granule-exocytosis killing
pathway. Depletion of T cells by injection of specific mAb had
no effect on the subsequent developing CD4 T cell response in the lungs
of BCG-infected mice, but significantly reduced cytotoxic activity and
IFN- production by lung CD8 T cells. Thus, T cells in the
lungs might help to control mycobacterial infection in the period
between innate and classical adaptive immunity and may also play an
important regulatory role in the subsequent onset of T
lymphocytes.
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