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

First Author  Kassiotis G Year  2001
Journal  J Neuroimmunol Volume  119
Issue  2 Pages  239-47
PubMed ID  11585627 Mgi Jnum  J:103105
Mgi Id  MGI:3608463 Doi  10.1016/s0165-5728(01)00403-9
Citation  Kassiotis G, et al. (2001) Defective CD4T cell priming and resistance to experimental autoimmune encephalomyelitis in TNF-deficient mice due to innate immune hypo-responsiveness. J Neuroimmunol 119(2):239-47
abstractText  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.
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