Alcoholic liver cirrhosis is associated with a decreased expression of theCD28 costimulatory molecule, a lower ability of T cells to bind exogenous IL-2, and increased soluble CD8 levels
Fj. Laso et al., Alcoholic liver cirrhosis is associated with a decreased expression of theCD28 costimulatory molecule, a lower ability of T cells to bind exogenous IL-2, and increased soluble CD8 levels, CYTOMETRY, 42(5), 2000, pp. 290-295
Despite the existence of high interleukin (IL)-12 serum levels in patients
with chronic active alcoholism, previous studies from our group have shown
that, during active ethanol intake, alcoholic patients with alcoholic liver
cirrhosis (ALC) display an impaired T-helper-l response together with abno
rmalities in the peripheral blood (PB) cytotoxic compartment. The aim of th
e present study was to gain further insights into the mechanisms underlying
these abnormalities, For that purpose, we analyzed the expression on PB B-
and T-cell subsets of both the CD28 and CD80 costimulatory molecules, the
ability of T lymphocytes to bind to exogenous recombinant IL-2, and the ser
um levels of soluble CD8 (sCD8) that might interfere with CD8+ T-cell activ
ation in a group of 10 ALC patients with active ethanol intake (ALCET group
). As reference groups, we analyzed 10 healthy individuals, 10 chronic alco
holic patients without liver disease (AWLD group) but with active ethanol i
ntake, and 10 ALC patients who had quit drinking for at least 1 year, Our r
esults showed that ALOFT patients display a significant decrease in the num
ber of PB CD28+/CD8(hi) T cells (P < 0.05) and CD80+ B cells (P < 0.01) com
pared with both healthy controls and AWLD patients, In addition, in ALOFT p
atients, PB T cells also showed a decreased ability to bind to exogenous IL
-2 (P < 0.01). This was associated with the existence of increased serum le
vels of sCD8 in ALC patients, the highest levels being detected in the ALOF
T group (P < 0.01). Altogether, our results point to the existence of sever
al abnormalities that would affect the cytotoxic response in ALOFT patients
. (C) 2000 Wiley-Liss, Inc.