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Blood, 15 August 2001, Vol. 98, No. 4, pp. 1108-1115
IMMUNOBIOLOGY
Tumor necrosis factor- induces coordinated changes in major
histocompatibility class I presentation pathway, resulting in increased
stability of class I complexes at the cell surface
Kristian Hallermalm,
Katzutake Seki,
Chenhong Wei,
Chiara Castelli,
Licia Rivoltini,
Rolf Kiessling, and
Jelena Levitskaya
From the Cancer Centrum Karolinska and the Microbiology
and Tumorbiology Center, Karolinska Institutet, Stockholm, Sweden; and
Unita Operativa Immunoterapia dei Tumori Umani, Istituto Nazionale
Tumori, Milan, Italy.
It is demonstrated that similar to interferon  (IFN-), tumor
necrosis factor- (TNF-) induces coordinated changes at different steps of the major histocompatibility complex (MHC) class I processing and presentation pathway in nonprofessional antigen-presenting cells
(APCs). TNF- up-regulates the expression of 3 catalytic immunoproteasome subunits LMP2, LMP7, and MECL-1the immunomodulatory proteasome activator PA28, the TAP1/TAP2 heterodimer, and the total
pool of MHC class I heavy chain. It was also found that in
TNF--treated cells, MHC class I molecules reconstitute more rapidly
and have an increased average half-life at the cell surface. Biochemical changes induced by TNF- in the MHC class I pathway were
translated into increased sensitivity of TNF--treated targets to
lysis by CD8+ cytotoxic T cells, demonstrating improved
presentation of at least certain endogenously processed MHC class
I-restricted peptide epitopes. Significantly, it was demonstrated that
the effects of TNF- observed in this experimental system were not
mediated through the induction of IFN-. It appears to be likely that
TNF--mediated effects on MHC class I processing and presentation do
not involve any intermediate messengers. Collectively, these data
demonstrate the existence of yet another biologic activity exerted by
TNF-, namely its capacity to act as a coordinated multi-step
modulator of the MHC class I pathway of antigen processing and
presentation. These results suggest that TNF- may be useful when a
concerted up-regulation of the MHC class I presentation machinery is
required but cannot be achieved by IFN-.
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