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Tumor necrosis factor ligand superfamily: involvement in the pathology of
malignant lymphomas
HJ Gruss and SK Dower
Department of Biochemistry, Immunex Research and Development Corp, Seattle,
WA, USA.
The TNF receptor superfamily members are all type I membrane glycoproteins
with typical homology in the extracellular domain of variable numbers of
cysteine-rich repeats (overall homologies, 25% to 30%). In contrast, the
TNF ligand superfamily members (with the exception of LT alpha) are type II
membrane glycoproteins with homology to TNF in the extracellular domain
(overall homologies, 20%). TNF and LT alpha are trimeric proteins and are
composed of beta-strands forming a beta-jellyroll. The homology of the
beta-strand regions for the TNF ligand superfamily members suggest a
similar beta-sandwich structure and possible trimeric or multimeric complex
formation for most or all members. A genetic linkage, as evidence for
evolutionary relatedness, is found by chromosomal cluster of TNFR p80,
CD30, 4-1BB, and OX40 for 1p36; TNFR p60, TNFR-RP, and CD27 for 12p13; TNF,
LT alpha, and LT beta for 6 (MHC locus); CD27L and 4-1BBL for 19p13; and
FASL and OX40L for 1q25. Of the TNF ligand superfamily, TNF, LT alpha, and
LT beta and their receptors (TNFR p60, TNFR p80, and TNFR-RP) interact in a
complex fashion of cross-binding. However, the other family members
presently have a one ligand/one receptor binding principle (CD27/CD27L,
CD30/CD30L, CD40/CD40L, 4-1BB/4-1BBL, OX40/gp34, and FAS/FASL). In general,
the members of the TNF ligand superfamily mediate interaction between
different hematopoietic cells, such as T cell/B cell, T cell/monocyte, and
T cell/T cell. Signals can be transduced not only through the receptors but
also through at least some of the ligands. The transduced signals can be
stimulatory or inhibitory depending on the target cell or the activation
state. Taken together, TNF superfamily ligands show for the immune response
an involvement in the induction of cytokine secretion and the upregulation
of adhesion molecules, activation antigens, and costimulatory proteins, all
known to amplify stimulatory and regulatory signals. On the other hand,
differences in the distribution, kinetics of induction, and requirements
for induction support a defined role for each of the ligands for
T-cell-mediated immune responses. The shedding of members of the TNF
receptor superfamily could limit the signals mediated by the corresponding
ligands as a functional regulatory mechanism. Induction of cytotoxic cell
death, observed for TNF, LT alpha, CD30L, CD95L, and 4-1BBL, is another
common functional feature of this cytokine family. Further studies have to
identify unique versus redundant biologic and physiologic functions for
each of the TNF superfamily ligands.(ABSTRACT TRUNCATED AT 400 WORDS)
Volume 85,
Issue 12,
pp. 3378-3404,
06/15/1995
Copyright © 1995 by The American Society of Hematology
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