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*
Centenary Institute of Cancer Medicine and Cell Biology, Newtown, Australia; and
Department of Medicine, University of Sydney, Sydney, Australia
Immune responses rely on an intricate system of adhesion molecules
to coordinate the homing and retention of lymphocytes in both secondary
lymphoid tissues and at sites of infection. To define the events
associated with pulmonary immune responses, the expression of
endothelial addressins and integrins on T cells was analyzed during
Mycobacterium tuberculosis infection. In infected lung,
expression of endothelial VCAM-1, but not mucosal addressin cell
adhesion molecule-1, was up-regulated from 4 wk postinfection and
persisted to at least 12 wk. Subsequent analysis of the corresponding
integrins expressed on lung CD4+ and CD8+ T
cells revealed an accumulation of
ß1high/ß7-/low,
and to a lesser extent ß7high,
integrin-expressing T cells during infection. Examination of integrin
heterodimers showed that while 
4 integrin was
predominantly expressed on
ß1high/ß7-/low
cells, E integrin was primarily associated with
ß7high. The majority of activated/memory T
cells recruited during infection expressed high levels of
ß1 integrin and undetectable or low levels of
ß7 integrin. These T cells were capable of producing
IFN-
, a cytokine crucial for controlling M.
tuberculosis infection. Rapid expansion of
ß1high, ß7-, and
ß7high T cell populations in the lung upon
secondary mycobacterial infection indicates the participation of these
populations in the acquired immune response to the infection.
Furthermore, treatment of infected mice with mAb to 4 or
4ß7 integrin led to a reduction in
lymphocytes and increase in granulocytes in the pulmonary infiltrate.
These results reveal a crucial role for adhesion molecules in the
generation of an effective pulmonary immune response to M.
tuberculosis infection.
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