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Promotes Humoral Autoimmunity by Preventing the Induction of CTL1
*
Research Service, Department of Veterans Affairs Medical Center and Division of Rheumatology and Clinical Immunology, University of Maryland School of Medicine, Baltimore, MD 21201; and
Immunology Division, Veterans Affairs Medical Center and University of Cincinnati College of Medicine, Cincinnati, OH 45267.
Neutralization of TNF-
in humans with rheumatoid arthritis or
Crohn’s disease has been associated with the development of humoral
autoimmunity. To determine the effect of TNF- neutralization on
cell-mediated and humoral-mediated responses, we administered
anti-TNF- mAb to mice undergoing acute graft-vs-host disease
(GVHD) using the parent-into-F1 model. In vivo
neutralization of TNF- blocked the lymphocytopenic features
characteristic of acute GVHD and induced a lupus-like chronic GVHD
phenotype (lymphoproliferation and autoantibody production). These
effects resulted from complete inhibition of detectable antihost CTL
activity and required the presence of anti-TNF- mAb for the
first 4 days after parental cell transfer, indicating that TNF-
plays a critical role in the induction of CTL. Moreover, an in vivo
blockade of TNF- preferentially inhibited the production of IFN-
and blocked IFN--dependent up-regulation of Fas; however, cytokines
such as IL-10, IL-6, or IL-4 were not inhibited. These results suggest
that a therapeutic TNF- blockade may promote humoral autoimmunity by
selectively inhibiting the induction of a CTL response that would
normally suppress autoreactive B cells.
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