Down-regulation of natural killer cells and of gamma/delta T cells in systemic lupus erythematosus. Does it correlate to autoimmunity and to laboratory indices of disease activity?
V. Riccieri et al., Down-regulation of natural killer cells and of gamma/delta T cells in systemic lupus erythematosus. Does it correlate to autoimmunity and to laboratory indices of disease activity?, LUPUS, 9(5), 2000, pp. 333-337
A depletion of natural killer (hTK) cells seems to play a role in the cours
e of systemic lupus erythematosus (SLE) whereas the possible involvement in
this disease of T cell receptor (TCR) gamma/delta positive T cells is stil
l debated.
The aim of this study was to evaluate the peripheral blood mononuclear cell
s (PBMCs) that express NK surface markers CD16 and CD56 or gamma/delta TCR
antigen in 58 SLE patients, investigating the possible role of these cell s
ubsets involved in non-MHC-restricted cytotoxicity and their relationship w
ith the main clinical and laboratory parameters.
SLE patients had, with respect to controls, considerably decreased values o
f NK cells (P < 0.0004 in percentage and P < 0.00004 as absolute number), o
f non-MHC-restricted T cytotoxic lymphocytes (P < 0.007 and P < 0.0015, res
pectively) and of T cells expressing gamma/delta TCR (P < 0.02 and P < 0.00
4, respectively). The absolute numbers of these cell subsets positively cor
related to each other (P < 0.009). gamma/delta T cells inversely correlated
with higher ESR values, both percentually (P < 0.006; r = -0.367) and in a
bsolute number (P < 0.009; r = -0.350). Moreover, the percentage values of
this cell subset inversely correlated with higher levels of CRP (P < 0.05;
r = -0.256) while SLE patients with anti-SSB/La antibodies had lower values
of T lymphocytes bearing gamma/delta TCR, both as percentage (P < 0.008) a
nd as absolute number (P < 0.02).
Our study indicates that non-MHC-restricted cytotoxicity, shared by NK, NK-
like and gamma/delta T cells, may be down-regulated in SLE patients, owing
to a significant reduction of these PBMC subsets. These specific cell subse
t impairments seem to affect only some aspects of the disease, suggesting a
weakening of the regulatory properties of these cells in the control of di
fferent immunological and inflammatory features of SLE, that could be of im
portance in its clinical expression.