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ß TCR+ Cells by Mycobacterium tuberculosis Via an Alternate Class I MHC Antigen-Processing Pathway1
Departments of
*
Medicine and
Pathology, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH 44106
Human immune responses to M. tuberculosis are
characterized by activation of multiple T cell subsets including
CD4+, CD8+, and 
T cells, and the role of
CD8+ 
ß TCR+ T cells in this response is
poorly understood. Stimulation of T cells from healthy tuberculin skin
test-positive persons with live M. tuberculosis-H37Ra or
soluble M. tuberculosis Ags readily up-regulated
IL-2R (CD25) expression on CD8+ T cells. Purified
resting and activated CD8+ T cells produced IFN- and
proliferated to both M. tuberculosis bacilli and soluble
mycobacterial Ags with monocytes as APC. Precursor frequency of
mycobacterial Ag-specific CD8+ T cells by IFN-
enzyme-linked immunospot was 5–10-fold lower than the precursor
frequency of CD4+ T cells, and IFN- secretion by
CD8+ T cells was 50–100-fold lower. CD8+ T
cells secreted 
10-fold less IFN- per cell than CD4+ T
cells in response to mycobacterial Ags. CD8+ T cell
responses to M. tuberculosis bacilli were blocked by
anti-MHC class I antibody and required Ag processing. Processing of
M. tuberculosis bacilli by monocytes for presentation to
MHC class I-restricted CD8+ T cells was insensitive to
brefeldin A treatment, which blocks the conventional MHC class I
Ag-processing pathway. These results represent the first demonstration
that human cells can process pathogen Ags via an alternate
Ag-processing pathway for MHC class I and suggest a mechanism for
participation of IFN--secreting CD8+ T cells in the
human immune responses to M.
tuberculosis.
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