M. Otsuka et al., EXPRESSION OF THE INTESTINAL T-LYMPHOCYTE-ASSOCIATED-MOLECULE RECOGNIZED BY THE HML-1 ANTIBODY ON MONONUCLEAR-CELLS FROM HPLV-I-INFECTED SUBJECTS, American journal of hematology, 50(1), 1995, pp. 1-8
We investigated the expression of a monoclonal antibody (HML-1) define
d antigen that appears on human intestinal T-lymphocytes in HTLV-l-rel
ated disease, We studied 25 ATL, and 24 healthy HTLV-I carriers, Patie
nts with acute ATL showed a variety of the expression of the HML-1 ant
igen (range 0.4-74.8%). HML-1 expression on mononuclear cells (MNCs) i
n blood from patients with chronic ATL ranged from 1.7-43.6% (mean 13.
5%). This level of expression was less than that of patients with acut
e ATL, but not significantly, In patients with smoldering ATL, the deg
ree of patients with acute ATL, but not significantly. In patients wit
h smoldering AIL, the degree of expression ranged from 1.6-13.3% (mean
8.0%). In contrast to patients with acute ATL, MNCs from patients wit
h acute myelogenous leukemia (AML), acute lymphocytic leukemia (ALL),
and B-cell type chronic lymphocytic leukemia (B-CLL) did not express t
he HML-1 antigen, except for the 2 patients with ALL. Healthy HTLV-I c
arriers and healthy controls also were negative for HML-1 reactivity.
In acute ATL, patients with gastrointestinal tract infiltration tended
to have high expression of the HML-1 epitope. After stimulation with
phytohemagglutinin (PHA), healthy HTLV-I carriers showed significantly
increased expression of the HML-1 epitope (P < 0.05). Recently, the b
eta 7 integrin family has been found to play a specific role in mucosa
l localization or adhesion, and HML-1 protein was found to match the d
educed beta 7 N-terminal sequence, We propose that the cellular gene r
esponsible for HML-1 epitope expression may, like IL-2, lL-2R, etc., b
e transactivated by infection with HTLV-I, and that HML-1 antigen gene
expression by HTLV-I infection may lead to infiltration of ATL cells
with highly expressed HML-1 epitope into the gut mucosa. (C) 1995 Wile
y-Liss, Inc.