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J Neuroimmunol. 2001 Oct 1;119(2):239-47.

Defective CD4T cell priming and resistance to experimental autoimmune encephalomyelitis in TNF-deficient mice due to innate immune hypo-responsiveness.

Author information

1
Institute for Immunology, Biomedical Sciences Research Center Alexander Fleming, Vari 166-72, Greece.

Abstract

We report here that tumor necrosis factor (TNF) deficiency causes innate hypo-responsiveness to a broad range of bacterial or viral constituents. In vivo hypo-responsiveness of TNF-deficient mice to mycobacteria results in defective CD4+ T cell priming to antigens administered in complete Freund's adjuvant (CFA). This deficiency is restored by supplementary mycobacteria. Furthermore, we show that even when self-reactive CD4+ T cell priming is fully restored, susceptibility of TNF-deficient mice to experimental autoimmune encephalomyelitis (EAE) depends on the co-administered pertussis toxin (PTx). TNF-deficient mice are completely resistant to EAE at sub-optimal doses of PTx, while supplementary PTx restores susceptibility. Therefore, TNF shows distinct functions in linking innate responsiveness to CD4+ T cell priming and to the induction of autoimmune disease.

PMID:
11585627
DOI:
10.1016/s0165-5728(01)00403-9
[Indexed for MEDLINE]

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