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The Journal of Immunology, Vol 157, Issue 4 1333-1336, Copyright © 1996 by American Association of Immunologists

CUTTING EDGE

CTLA-4 blockade enhances clinical disease and cytokine production during experimental allergic encephalomyelitis

PJ Perrin, JH Maldonado, TA Davis, CH June and MK Racke
Immune Cell Biology Program, Naval Medical Research Institute, Bethesda, MD 20889-5607, USA. rinOpjp@bumed30.med.navy.mil

The B7 family of cell surface molecules expressed on APC provides accessory signals to T cells via either CD28 or CTLA-4. However, while CD28 transduces a costimulatory signal that is required for an optimal immune response, CTLA-4 transmits a negative signal. These studies use an anti-CTLA-4 mAb to directly address the role of this T cell surface molecule in experimental allergic encephalomyelitis (EAE). CTLA-4 regulation of disease was assessed during initial immune cell interactions and during the effector stage of the encephalitogenic immune response. The effects of anti-CTLA-4 treatment were schedule dependent. CTLA-4 blockade during the onset of clinical symptoms markedly exacerbated disease, enhancing mortality. Disease exacerbation was associated with enhanced production of the encephalitogenic cytokines TNF-alpha, IFN-gamma and IL-2. Hence, CTLA-4 regulates the intensity of the autoimmune response in EAE, attenuating inflammatory cytokine production and clinical disease manifestations.


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