By Frederick W. Alt
Advances in Immunology , a fashioned and hugely revered booklet, provides present advancements in addition to accomplished experiences in immunology. Articles tackle the wide variety of subject matters that include immunology, together with molecular and mobile activation mechanisms, phylogeny and molecular evolution, and medical modalities. Edited and authored by means of the main scientists within the box, each one quantity offers up to date info and instructions for destiny examine.
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Additional info for Advances in Immunology, Vol. 96
Sample text
2006a). Severe disease, unaltered leukocyte migration, and reduced IFN-gamma production in CXCR3À/À mice with experimental autoimmune encephalomyelitis. J. Immunol. 176, 4399–4409. , and Issazadeh-Navikas, S. (2006b). Neuron-mediated generation of regulatory T cells from encephalitogenic T cells suppresses EAE. Nat. Med. 12, 518–525. Lucchinetti, C. , Mandler, R. , Ransohoff, R. , Parisi, J. , and Lassmann, H. (2002). A role for humoral mechanisms in the pathogenesis of Devic’s neuromyelitis optica.
2000), but their relevance for the therapeutic effect of leflunomide is unclear. , 2002). , 2004). , 2006). A Phase III clinical trial is currently being conducted to test efficiency and adverse effects on a larger clinical scale. 4. , 1999). , 2002). , 2000) delayed its introduction into clinical practice. This effect had not been observed in EAE, as CD40L is not expressed on murine but on human platelets. As a result, new trials with coadministration of heparin were initiated and are still running.
Antel, J. , et al. (2006). Natalizumab effects on immune cell responses in multiple sclerosis. Ann. Neurol. 59, 748–754. , Deisz, R. , Lehmann, T. , and Zipp, F. (2000). Human brain-cell death induced by tumour-necrosis-factor-related apoptosisinducing ligand (TRAIL). Lancet 356, 827–828. , Pfueller, C. , and Kamradt, T. (2005). Lipopolysaccharide injection induces relapses of experimental autoimmune encephalomyelitis in nontransgenic mice via bystander activation of autoreactive CD4þ cells. J.
