SYSTEMIC lupus erythematosus (SLE) is a disorder with a wide range of immun
ological abnormalities. The results of the studies undertaken ill the last
decade indicated that SLE pathogenesis was mainly connected with the breakd
own of the activation control of B and T cells, generating humoral or cell-
mediated responses against several self-antigens of affected cells. The las
t studies demonstrate that the role of gamma delta T lymphocytes in autoimm
une diseases can be especially important. Flow cytometry techniques were us
ed to investigate the number and percentage of TCR gamma delta T cells and
their most frequent subtypes in peripheral. blood of 32 patients with SLE a
nd 16 healthy volunteers. We also correlated TCR ya cells number with the l
evel of T CD3(+), T CD4(+), T CD8(+), and NK (CD16) cells (cytometric measu
rements) and SLE activity (on the basis of clinical investigations). Our st
udies were preliminary attempts to evaluate the role of that minor T cell s
ubpopulation in SLE. Absolute numbers of cells expressing gamma delta TCR i
n most SLE blood specimens were significantly lower than in the control gro
up (P<0.006). However, since the level of total T cell population was also
decreased in the case of SLE, the mean values of the percentage gamma delta
T cells of pan T lymphocytes were almost the same in both analysed populat
ions (7.1% vs 6.3%, respectively). In contrast to V delta 2(+) and V gamma
9(+) subtypes of pan gamma delta T cells, V delta 3(+) T cells number was h
igher in SLE patients (20 x 10 cells/mu l) than in healthy control group (2
x 2 cells/mu l) (P=0.001). However, we found no differences between the nu
mbers of pan gamma delta T lymphocytes and studied their subtypes in the pa
tients with active and inactive disease. These cell subpopulations were dou
bled In the treated patients with immunosuppressive agents In comparison wi
th untreated ones; however, data were not statistically significant. Our st
udy indicated that V delta 3(+) subtype of gamma delta T cells seems to be
involved in SLE pathogenesis; however, we accept the idea that the autoimmu
nity does not develop from a single abnormality, but rather from a number o
f different events.