KERATINOCYTE-LYMPHOCYTE INTERACTION IN CUTANEOUS T-CELL LYMPHOMA - MODULATION OF KERATINOCYTE ANTIGEN MY7 BY A SOLUBLE FACTOR PRODUCED BY T-LYMPHOCYTES
P. Celerier et al., KERATINOCYTE-LYMPHOCYTE INTERACTION IN CUTANEOUS T-CELL LYMPHOMA - MODULATION OF KERATINOCYTE ANTIGEN MY7 BY A SOLUBLE FACTOR PRODUCED BY T-LYMPHOCYTES, Archives of dermatology, 133(7), 1997, pp. 837-840
Objective: To test the hypothesis that the modulation of My7 antigen i
n the basal keratinocytes is directly related to the effect of dermal
lymphocyte infiltrate of epidermotropic cutaneous T-cell lymphoma (CTC
L). Design: In vitro study with reconstituted skin model. Setting: Dep
artment of Dermatology of Universitary Hospital, Nantes, France. Patie
nts: Lymphocytes extracted from 11 skin samples with lesions of epider
motropic CTCL (mycosis fungoides, stages Ila to IV) and 6 skin samples
with lesions of atopic dermatitis (control population) together with
the supernatants of these infiltrating lymphocytes were incubated with
normal reconstituted skin samples either alone or in the presence of
interferon alfa-2a (10(2) IU/mL). Moreover, normal peripheral blood mo
nonuclear cells of 7 patients and 4 controls were incubated with re co
nstituted skin. Intervention: None. Main Outcome Measures: None. Resul
ts: Ten of 11 samples of lymphocytes extracted from CTCL and 7 of 11 o
f their supernatants inhibited partially or completely My7 expression
by basal cells. No inhibition was noted for lymphocytes extracted from
inflammatory skin or their supernatants. Addition of interferon alfa-
2a in a culture medium of extracted lymphocytes or their supernatants
blocked inhibition of My7 expression by keratinocytes in 8 of 10 recon
stituted skin samples. No abrogation of My7 expression was noted with
peripheral mononuclear cells. Conclusions: Our in vitro study demonstr
ated a direct and specific interaction between the tumor infiltrate of
CTCL and keratinocytes. Moreover, this interaction appeared to be clo
sely associated with a soluble factor produced by the tumor T-cell inf
iltrate and was at least partially blocked by interferon alfa-2a.