Interaction between apoptotic cells and reactive brain cells in the central nervous system of rats with autoimmune encephalomyelitis

Kohji, Toshihiko; Tanuma, Naoyuki; Aikawa, Yukihiko; Kawazoe, Yoshimasa; Suzuki, Yoko; Kohyama, Kuniko; Matsumoto, Yoh

doi:10.1016/s0165-5728(97)00198-7

Cited by 34 publications

(21 citation statements)

References 22 publications

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“…These factors probably affect the number of infected/activated T cells infiltrating the CNS and the extent of migration of these cells through the CNS parenchyma (61,62,64). Once in the CNS, Tax-expressing T lymphocytes may persist and expand within the CNS, as Tax is able to prevent T cells from undergoing apoptosis (44) that may be stimulated by neighboring astrocytes (32). In conclusion, our results demonstrate a great susceptibility of astrocytes vis-à-vis HTLV-1-infected T cells, which significantly alters the metabolism of an important excitatory amino acid, glutamate.…”

Section: Discussionmentioning

confidence: 99%

Human T-Cell Lymphotropic Virus Type 1-Infected T Lymphocytes Impair Catabolism and Uptake of Glutamate by Astrocytes via Tax-1 and Tumor Necrosis Factor Alpha

Szymocha

Akaoka

Dutuit

et al. 2000

J Virol

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Section: Discussionmentioning

confidence: 99%

Human T-Cell Lymphotropic Virus Type 1-Infected T Lymphocytes Impair Catabolism and Uptake of Glutamate by Astrocytes via Tax-1 and Tumor Necrosis Factor Alpha

Szymocha

Akaoka

Dutuit

et al. 2000

J Virol

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“…The clinical severity of EAE was divided into four stages (grade 1, floppy tail; grade 2, mild paraparesis; grade 3, severe paraparesis; grade 4, tetraparesis or moribund condition) [24]. The clinical course of acute and chronic relapsing EAE was shown in the previous study [25]. In this study, tissue sampling was performed at the early (day 10-12 PI, grade 1), peak (day 13-15 PI, grade 3-4) and recovery (day 21-23 PI, grade 0) stages of acute EAE and at the 1st attack (day 14-17 PI, grade 3-4), remission (day 20-23 PI, grade 0), 2nd attack (day 25-27 PI, grade 3) and full recovery stage (day 34-37 PI, grade 0) of chronic relapsing EAE.…”

Section: Rats and Eae Inductionmentioning

confidence: 99%

Diagnosis and assessment of preclinical and clinical autoimmune encephalomyelitis using peripheral blood lymphocyte TCR

et al. 1998

Self Cite

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In organ-specific autoimmune diseases, T cells involved in the disease development bear a particular type of TCR and infiltrate the target organ predominantly. However, it is difficult to identify disease-inducing T cells in peripheral blood lymphocytes (PBL) because such T cells are very few in number in a large pool of unrelated T cells. In the present study, we demonstrate that CDR3 spectratyping can identify experimental autoimmune encephalomyelitis (EAE)-specific patterns (oligoclonal expansion of Vbeta8.2 with the shortest CDR3) in PBL at the preclinical and clinical stages of acute EAE. Analysis of nucleotide and predicted amino acid sequences of Vbeta8.2 CDR3 of spectratype-derived clones revealed that CASSDSSYEQYFGPG, which is one of the representative sequences of encephalitogenic T cell clones, constituted the predominant population in both PBL and spinal cord T cells. In chronic relapsing EAE, the EAE-specific spectratype pattern in PBL was observed during the 1 st and 2nd attacks, but not at the remission and full recovery stage. These findings indicate that the spectratyping pattern in PBL reflects the disease activity of acute and chronic relapsing EAE. Thus, CDR3 spectratyping using PBL can be used for diagnosis and assessment of T cell-mediated autoimmune diseases and is applicable to human autoimmune diseases.

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“…In the central nervous system of rats with autoimmune encephalomyelitis, apoptotic cells were detected on postimmunization (PI) days 10-12, increased and peaked at PI day 13. Then these cells decreased gradually by PI day 21 [23]. Thus, time course examination of ganglion neurons might provide a better understanding of the neuronal degeneration within the spiral ganglion in AIED.…”

Section: Discussionmentioning

confidence: 95%

TUNEL-Positive Labeling in Mouse Inner Ear Caused by Tubulin Immunization Is Not Apoptosis

Mora²,

Barbieri³

et al. 2003

ORL

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Apoptosis is involved in all fundamental processes of the immune system. To study whether apoptosis plays any role in the pathogenesis of autoimmune inner ear disease, we immunized Balb/c mice with tubulin. The inner ears were examined with TUNEL (in situ terminal dUTP nick-end labeling) and immunocytochemistry of the apoptosis regulatory proteins Bcl-2 and Bax. TUNEL-positive cells are found in the tubulin-immunized inner ears but not in the control inner ears. The positive cells are the marginal cells in the stria vascularis, and the hair cells in Corti’s organ and the saccule. However, under morphological analysis by light microscope, these cells lack the features characteristic of apoptosis. Moreover, no cells staining positive for Bcl-2 and Bax are found in any structures of the inner ears. These results suggest that positive TUNEL staining in this model does not indicate apoptosis and apoptosis may be not involved in autoimmune inner ear disease.

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Interaction between apoptotic cells and reactive brain cells in the central nervous system of rats with autoimmune encephalomyelitis

Cited by 34 publications

References 22 publications

Human T-Cell Lymphotropic Virus Type 1-Infected T Lymphocytes Impair Catabolism and Uptake of Glutamate by Astrocytes via Tax-1 and Tumor Necrosis Factor Alpha

Human T-Cell Lymphotropic Virus Type 1-Infected T Lymphocytes Impair Catabolism and Uptake of Glutamate by Astrocytes via Tax-1 and Tumor Necrosis Factor Alpha

Diagnosis and assessment of preclinical and clinical autoimmune encephalomyelitis using peripheral blood lymphocyte TCR

TUNEL-Positive Labeling in Mouse Inner Ear Caused by Tubulin Immunization Is Not Apoptosis

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