Persistence of an encephalitogenic T cell clone in the spinal cord during chronic, relapsing experimental autoimmune encephalomyelitis

Fritz, Robert B.; Russell, James P.; Zhao, Ming-Lang

doi:10.1016/s0165-5728(98)00034-4

Cited by 6 publications

(6 citation statements)

References 24 publications

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“…The CD3 signal was normalized to the HPRT signal and was found to be stronger during disease stages and reduced at remission. This finding is consistent with our recent report that an encephalitogenic T cell clone was readily detected in the spinal cord during the acute and relapse stages of disease, but was not found during remission (10). Others have reported a decrease in CNS T cell number following acute EAE (17,18).…”

Section: Discussionsupporting

confidence: 93%

“…Interestingly, the SJL T cell clone used in the present experiments also had a very short CDR3 region; however, in the mouse model, the CDR3 regions of the TCR B chains of encephalitogenic T cells are more diverse with respect to size and VB family (10).…”

Section: Discussionmentioning

confidence: 90%

“…We recently reported that when EAE was induced by a single T cell clone, the clone could be detected in the spinal cord during disease phases, but not during remissions (10). As a TCR molecular idiotypic marker was used to identify the donor clone after transfer to the recipients, no information was available with respect to other T cells that might be present in the spinal cord at these times.…”

Section: Resultsmentioning

confidence: 99%

“…Recently, we generated several encephalitogenic PLP peptide 139 -151-specific T cell clones, and found that by using the CDR3 region of one of these T cell clones, 3-19, as an idiotypic marker, the clone could be tracked in the CNS during the acute and relapse phases of EAE (3,10). It also allowed ready differentiation of the clone from host-derived T cells, as the marker was unique to the clone.…”

Section: E Xperimental Autoimmune Encephalomyelitis (Eae)mentioning

confidence: 99%

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Alterations in the Spinal Cord T Cell Repertoire During Relapsing Experimental Autoimmune Encephalomyelitis

Fritz

Wang

Zhao

2000

The Journal of Immunology

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The CNS T cell repertoire was analyzed by RT-PCR, spectratyping, and nucleotide sequencing of the amplified products at different times following adoptive transfer of a CD4+, Th1, VB2+ encephalitogenic SJL/J proteolipid protein peptide 139–151-specific T cell clone. The third complementarity-determining region of TCR B chains in the spinal cord was used as an indicator of T cell heterogeneity. Spectratypic analysis revealed that a single peak corresponding to the third complementarity-determining region of the initiating T cell clone predominated during the acute phase. During recovery and relapse the complexity of the spectratype increased. DNA sequence analysis revealed that the donor clone predominated at the acute phase. By the first relapse the donor clone, although represented most frequently, was a minority of the total. Spectratypic analysis of the same samples for several other VB families revealed their presence during acute disease or relapses but, with the exception of VB17, their absence during the recovery stage.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 90%

Section: Resultsmentioning

confidence: 99%

Section: E Xperimental Autoimmune Encephalomyelitis (Eae)mentioning

confidence: 99%

See 2 more Smart Citations

Alterations in the Spinal Cord T Cell Repertoire During Relapsing Experimental Autoimmune Encephalomyelitis

Fritz

Wang

Zhao

2000

The Journal of Immunology

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“…As a less popular alternative, sequential disease episodes could be driven by members of the initial pathogenic clone(s) throughout the entire course of disease. Such a pathogenesis would invoke formation and persistence of autoimmune memory T cells (8).…”

mentioning

confidence: 99%

Autoimmune CD4+ T Cell Memory: Lifelong Persistence of Encephalitogenic T Cell Clones in Healthy Immune Repertoires

Kawakami

Odoardi

Ziemssen

et al. 2005

The Journal of Immunology

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We embedded green fluorescent CD4+ T cells specific for myelin basic protein (MBP) (TMBP-GFP cells) in the immune system of syngeneic neonatal rats. These cells persisted in the animals for the entire observation period spanning >2 years without affecting the health of the hosts. They maintained a memory phenotype with low levels of L-selectin and CD45RC, but high CD44. Although persisting in low numbers (0.01–0.1% of lymph node cells) they were sufficient to raise susceptibility toward clinical autoimmune disease. Immunization with MBP in IFA induced CNS inflammation and overt clinical disease in animals carrying neonatally transferred TMBP-GFP cells, but not in controls. The onset of the clinical disease coincided with mass infiltration of TMBP-GFP cells into the CNS. In the periphery, following the amplification phase a rapid contraction of the T cell population was observed. However, elevated numbers of fully reactive TMBP-GFP cells remained in the peripheral immune system after acute experimental autoimmune encephalomyelitis mediating reimmunization-induced disease relapses.

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2006

McAlpine's Multiple Sclerosis

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Persistence of an encephalitogenic T cell clone in the spinal cord during chronic, relapsing experimental autoimmune encephalomyelitis

Cited by 6 publications

References 24 publications

Alterations in the Spinal Cord T Cell Repertoire During Relapsing Experimental Autoimmune Encephalomyelitis

Alterations in the Spinal Cord T Cell Repertoire During Relapsing Experimental Autoimmune Encephalomyelitis

Autoimmune CD4+ T Cell Memory: Lifelong Persistence of Encephalitogenic T Cell Clones in Healthy Immune Repertoires

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