encephalitogenic

en·ceph·a·li·to·gen·ic

(en-sef'ă-li-tō-jen'ik),
Producing encephalitis; typically by hypersensitivity mechanisms. See: encephalitogen.

encephalitogenic

/en·ceph·a·lit·o·gen·ic/ (en-sef″ah-lit-o-jen´ik) causing encephalitis.

en·ceph·a·li·to·gen·ic

(en-sef'ă-li-tō-jen'ik)
Producing encephalitis; typically by hypersensitivity mechanisms.
References in periodicals archive ?
Antibodies to neuron-specific antigens in children with autism: possible cross-reaction with encephalitogenic proteins from milk, Chlamydia pneumoniae and Streptococcus Group A.
The t regs stimulated by GA may crossreact with myelin within the nervous system to turn off encephalitogenic effector T cells.
Durelli presented an Italian multicentre study which showed that interleukin IL-17 and IL-22 were increased in MS relapses and their specificity for a myelin antigen suggests that it may be encephalitogenic.
Dendritic cells pulsed (incubated) with encephalitogenic or nonencephalitogenic peptides derived from myelin basic protein when administered intravenously or locally to the site of injury, promoted recovery from SCI (102).
Emerging encephalitogenic viruses: lyssaviruses and henipaviruses transmitted by frugivorous bats.
EAE is induced by immunization with myelin, myelin proteins, and myelin protein encephalitogenic epitopes or by the passive transfer of myelin-reactive cluster of differentiation (CD) 4 cells.
Myelin encephalitogenic protein fragments in cerebrospinal fluid of persons with multiple sclerosis.
Fitzgerald DC, Ciric B, Touil T, Harle H, Grammatikopolou J, Das Sarma J, et al, Suppressive effect of IL-27 on encephalitogenic Th17 cells and the effector phase of experimental autoimmune encephalomyelitis.
When T-cell lines are not available, inflammation can also be induced by active sensitization with an encephalitogenic peptide; however, the more pronounced variability of EAE in an active model may mask additional effects, induced by antibodies, in particular when they are subtle.
K+ channel-blocking alkoxypsoralens inhibit the immune response of encephalitogenic T line cells and lymphocytes from Lewis rats challenged for experimental autoimmune encephalomyelitis.
The third presentation gives an overview of the mechanisms of genetic changes and neurovirulence of encephalitogenic arboviruses.
Certainly, the most exciting development in MS therapy during the last few years is the approval of the humanized monoclonal antibody (mAb) natalizumab which targets [alpha]4[beta]1-integrin (VLA-4) on the surface of encephalitogenic leukocytes.