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Blood, 1 December 2001, Vol. 98, No. 12, pp. 3465-3472
TRANSPLANTATION
Immunosuppressive properties of CD95L-transduced
"killer" hybrids created by fusing donor- and recipient-derived
dendritic cells
Hiroyuki Matsue,
Keiko Matsue,
Masahiro Kusuhara,
Tadashi Kumamoto,
Ko Okumura,
Hideo Yagita, and
Akira Takashima
From the Department of Dermatology, University of Texas
Southwestern Medical Center, Dallas; the Department of Immunology,
Juntendo University School of Medicine, Tokyo, Japan; and Core Research
for Evolutional Science and Technology (CREST), Japan Science
and Technology Corporation, Tokyo, Japan.
Allogeneic immune responses, which are initiated by dendritic cells
(DCs) of both donor and host origins, remain a major obstacle in organ
transplantation. Presentation of intact major histocompatibility complex (MHC) molecules by allogeneic DCs and allogeneic peptides by
syngeneic DCs leads to complex allogeneic immune responses. This study
reports a novel strategy designed to suppress both pathways. A stable
DC line XS106 (A/J mouse origin) was transfected with CD95L cDNA and
fused with splenic DCs purified from allogeneic BALB/c mice. The
resulting "killer" DC-DC hybrids: (1) expressed CD95L and
MHC class I and class II molecules of both A/J and BALB/c origins,
while maintaining otherwise characteristic surface phenotypes of mature
DCs; (2) inhibited MHC class I- and class II-restricted mixed leukocyte reactions between the parental strains by triggering apoptosis of alloreactive T cells; and (3) abolished delayed-type hypersensitivity responses of A/J (and BALB/c) mice to
BALB/c-associated (and A/J-associated) alloantigens when injected
intravenously into A/J (and BALB/c) mice. The onset of
graft-versus-host disease in (BALB/c × A/J) F1 hosts
receiving A/J-derived hematopoietic cell transplantation was suppressed
significantly (P < .001) by killer DC-DC hybrid
treatment. These results form both technical and conceptual frameworks
for clinical applications of CD95L-transduced killer hybrids created
between donor DCs and recipient DCs in the prevention of allogeneic
immune responses following organ transplantation.
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