This antiself reactivity might serve to amplify the intensity of white matter damage.However, a parallel antiself reactivity has not been reproducibly described in the MHV model, and, therefore, it does not appear to be requisite for demyelination.Moreover, the MHV model presents an interesting challenge in answering the central question concerning what are the mechanisms of viral RNA persistent in the absenceof viral replication.A thorough analysis the selective contributions T cells to inflammation and demyelination following virus.The data suggest distinct roles for each T cell disease pathology.RS: Molecular FASEB J, mimicry. a mechanism for In retinal ischemia, we show early, transient upregulation of TNF, TNF receptor, and TNFR hr after reperfusion preceding neuronal cell loss.To assess the specic role of TNF and its receptors, we compared ischemiareperfusioninduced retinal damage in mice decient for TNFR, TNFR, or TNF by quantifying neuronal cell loss dafter the insult.Selective inhibition of TNFR function may represent a new approach to reduce ischemiainduced neuronal damage, being potentially superior to strategies aimed at suppression of TNF activity in general.Retinalischemiais a frequent complication in diabetic patients andis believed to represent many aspects of other brainischemic insults.Development of a brainischemic lesion depends on the acti vation of many pathophysiological processes, dominating basal or concomitantly induced neuroprotecti ve mechani sms. Production and release ofcy tokines, particularly of TN F,is one of the early cellular events subsequent to anischemic epi sode. Because of its di verse bioactivities, itis presently not clear under which conditions TN F promotes benecial or deleterious effects on neuronal ti ssues.An answer to thisquestion might prov ide new strategies to prevent pathologies resulting fromischemia.bacterial responses and in determining sensitivityto septic shock syndromes andis involved in the cellular organization of secondarylymphoid ti ssues. The role of TN FR was unclear until the membrane form of TN F was recognized as the physiological acti vator of thisTN F receptor. Several studies now point to an important contribution of TN FR to immune cell acti vation and endothelialfunctions, based on a cooperati ve actionwith TN FR. For immunohi stologyand immunoblotting, animals werekilled a fter or hr of reperf usion and Flurbiprofen immediately enucleated.Forischemic damage analysi s, left eyes were removed a fter dof reperfusion.For comparati ve purposes, noni schemic retinas from each mouse strain were also investigated.LY was di ssolved in DMSO at mg ml diluted to M in. A fter washing, diamidinophenylindole dihydrochlor ide was applied for min.Retinas were examined by standard immunouorescent microscopy.The specicityof each of the TN F TN R antibodies was checked and ver ied by complete lack of staining in the respecti ve knockout strain.Histolog ical Riboflavin procedures and quantication of ischemic damage.Eyes were xed for hr in para formaldehyde, dehydrated, and embedded in para fn.Sections containing the retina and crossing the optic ner ve were stainedwith hematox ylin and eosin.They were ex pressed as a number of nuclei in a mw ide band for the outer and inner nuclear layers and as a number of nuclei in a mw ide band for the ganglion cell layer.Retinal sections were examined from digitalized images.