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From the Department of Laboratory Medicine,*
Vaccine/Virology Division, Retrovirology Laboratory, Seattle,
University of Washington School of Medicine, Washington; the Department
of Laboratory Medicine,
Yale University, New
Haven, Connecticut; and the Department of Pulmonary and Mediastinal
Pathology,
Armed Forces Institute of
Pathology, Washington, D.C.
Because the mechanisms of lymphocyte accumulation in the lungs of
children with AIDS-associated lymphocytic interstitial pneumonia (LIP)
are unknown, we studied the relative contributions of known
adhesion pathways in mediating lymphocyte adherence to endothelium and
the potential role of human herpesviruses in the expansion of these
lesions. LIP was characterized by lymphoid hyperplasia of the
bronchus-associated lymphoid tissue (BALT) and infiltration of the
pulmonary interstitium with CD8+ T lymphocytes. In some
individuals there was expansion of the alveolar septae with dense
aggregates of B lymphocytes, many containing the Epstein-Barr
viral (EBV) genome. Patients with concurrent EBV infection also
demonstrated large-vessel arteriopathy characterized by thickening of
the intimae with collagen and smooth muscle. Venular endothelium from
the lung of children with LIP, but not uninflamed lung from
other children with AIDS or lung from children with nonspecific
pneumonitis, expressed high levels of vascular cell adhesion
molecule-1 (VCAM-1) protein. In turn, inflammatory cells
expressing very late activation antigen-4 (VLA-4), the
leukocyte ligand for VCAM-1, were the predominant perivascular
infiltrate associated with vessels expressing VCAM-1. Expression of
other endothelial adhesion molecules, including intracellular
adhesion molecule-1 and E-selectin, was not uniformly
associated with LIP. Using a tissue adhesion assay combined with
immunohistochemistry for VCAM-1, we show that CD8+
T cell clones that express VLA-4 bind preferentially to pulmonary
vessels in sites of LIP: vessels that expressed high levels of VCAM-1.
When tissues and cells were pretreated with antibodies to VCAM-1 or
VLA-4, respectively, adhesion was inhibited by 
80%.
Thus, infiltration of alveolar septae with CD8+ T
cells was highly correlative with VCAM-1/VLA-4 adhesive
interactions, and focal expansion of B cells was coincidental
to co-infection with EBV.
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