The Experts below are selected from a list of 693 Experts worldwide ranked by ideXlab platform
Joyce A Deleo - One of the best experts on this subject based on the ideXlab platform.
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cns infiltrating cd4 t Lymphocytes contribute to murine spinal nerve transection induced neuropathic pain
European Journal of Immunology, 2008Co-Authors: Joyce A DeleoAbstract:We previously reported leukocytic infiltration into the Lumbar spinal cord in a rodent spinal nerve L5 transection (L5Tx) neuropathic pain model. Here, we further investigated the role of infiltrating T Lymphocytes in the etiology of persistent pain following L5Tx. T Lymphocyte-deficient nude mice showed no evident mechanical hypersensitivity after day 3 of L5Tx compared to wild-type BALB/c mice. Through FACS analysis, we determined that significant leukocytic infiltration (CD45hi) into the Lumbar spinal cord peaked at day 7 post L5Tx. These infiltrating leukocytes contained predominantly CD4+ but not CD8+ T Lymphocytes. B Lymphocytes, natural killer cells and macrophages were not detected at day 7 post L5Tx. No differences in the activation of peripheral CD4+ T Lymphocytes were detected in either the spleen or Lumbar Lymph Nodes between L5Tx and sham surgery groups. Further, CD4 KO mice displayed significantly decreased mechanical hypersensitivity after day 7 of L5Tx, and adoptive transfer of CD4+ leukocytes reversed this effect. Decreased immunoreactivity of glial fibrillary acidic protein observed in CD4 KO mice post L5Tx indicated possible T Lymphocyte-glial interactions. These results strongly support a contributing role of spinal cord-infiltrating CD4+ T Lymphocytes versus peripheral CD4+ T Lymphocytes in the maintenance of nerve injury-induced neuropathic pain.
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CNS‐infiltrating CD4+ T Lymphocytes contribute to murine spinal nerve transection‐induced neuropathic pain
European journal of immunology, 2008Co-Authors: Ling Cao, Joyce A DeleoAbstract:We previously reported leukocytic infiltration into the Lumbar spinal cord in a rodent spinal nerve L5 transection (L5Tx) neuropathic pain model. Here, we further investigated the role of infiltrating T Lymphocytes in the etiology of persistent pain following L5Tx. T Lymphocyte-deficient nude mice showed no evident mechanical hypersensitivity after day 3 of L5Tx compared to wild-type BALB/c mice. Through FACS analysis, we determined that significant leukocytic infiltration (CD45(hi)) into the Lumbar spinal cord peaked at day 7 post L5Tx. These infiltrating leukocytes contained predominantly CD4(+) but not CD8(+) T Lymphocytes. B Lymphocytes, natural killer cells and macrophages were not detected at day 7 post L5Tx. No differences in the activation of peripheral CD4(+) T Lymphocytes were detected in either the spleen or Lumbar Lymph Nodes between L5Tx and sham surgery groups. Further, CD4 KO mice displayed significantly decreased mechanical hypersensitivity after day 7 of L5Tx, and adoptive transfer of CD4(+) leukocytes reversed this effect. Decreased immunoreactivity of glial fibrillary acidic protein observed in CD4 KO mice post L5Tx indicated possible T Lymphocyte-glial interactions. These results strongly support a contributing role of spinal cord-infiltrating CD4(+) T Lymphocytes versus peripheral CD4(+) T Lymphocytes in the maintenance of nerve injury-induced neuropathic pain.
Hong-yi Ren - One of the best experts on this subject based on the ideXlab platform.
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CD4+ αβ T cell infiltration into the leptomeninges of Lumbar dorsal roots contributes to the transition from acute to chronic mechanical allodynia after adult rat tibial nerve injuries.
Journal of neuroinflammation, 2018Co-Authors: You-quan Ding, Xia Xiao, Hong-yi RenAbstract:Antigen-specific and MHCII-restricted CD4+ αβ T cells have been shown or suggested to play an important role in the transition from acute to chronic mechanical allodynia after peripheral nerve injuries. However, it is still largely unknown where these T cells infiltrate along the somatosensory pathways transmitting mechanical allodynia to initiate the development of chronic mechanical allodynia after nerve injuries. Therefore, the purpose of this study was to ascertain the definite neuroimmune interface for these T cells to initiate the development of chronic mechanical allodynia after peripheral nerve injuries. First, we utilized both chromogenic and fluorescent immunohistochemistry (IHC) to map αβ T cells along the somatosensory pathways for the transmission of mechanical allodynia after modified spared nerve injuries (mSNIs), i.e., tibial nerve injuries, in adult male Sprague-Dawley rats. We further characterized the molecular identity of these αβ T cells selectively infiltrating into the leptomeninges of L4 dorsal roots (DRs). Second, we identified the specific origins in Lumbar Lymph Nodes (LLNs) for CD4+ αβ T cells selectively present in the leptomeninges of L4 DRs by two experiments: (1) chromogenic IHC in these Lymph Nodes for CD4+ αβ T cell responses after mSNIs and (2) fluorescent IHC for temporal dynamics of CD4+ αβ T cell infiltration into the L4 DR leptomeninges after mSNIs in prior Lymphadenectomized or sham-operated animals to LLNs. Finally, following mSNIs, we evaluated the effects of region-specific targeting of these T cells through prior Lymphadenectomy to LLNs and chronic intrathecal application of the suppressive anti-αβTCR antibodies on the development of mechanical allodynia by von Frey hair test and spinal glial or neuronal activation by fluorescent IHC. Our results showed that during the sub-acute phase after mSNIs, αβ T cells selectively infiltrate into the leptomeninges of the Lumbar DRs along the somatosensory pathways responsible for transmitting mechanical allodynia. Almost all these αβ T cells are CD4 positive. Moreover, the temporal dynamics of CD4+ αβ T cell infiltration into the Lumbar DR leptomeninges are specifically determined by LLNs after mSNIs. Prior Lymphadenectomy to LLNs specifically reduces the development of mSNI-induced chronic mechanical allodynia. More importantly, intrathecal application of the suppressive anti-αβTCR antibodies reduces the development of mSNI-induced chronic mechanical allodynia. In addition, prior Lymphadenectomy to LLNs attenuates mSNI-induced spinal activation of glial cells and PKCγ+ excitatory interneurons. The noteworthy results here provide the first evidence that CD4+ αβ T cells selectively infiltrate into the DR leptomeninges of the somatosensory pathways transmitting mechanical allodynia and contribute to the transition from acute to chronic mechanical allodynia after peripheral nerve injuries.
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CD4+ αβ T cell infiltration into the leptomeninges of Lumbar dorsal roots contributes to the transition from acute to chronic mechanical allodynia after adult rat tibial nerve injuries
BMC, 2018Co-Authors: You-quan Ding, Xia Xiao, Hong-yi RenAbstract:Abstract Background Antigen-specific and MHCII-restricted CD4+ αβ T cells have been shown or suggested to play an important role in the transition from acute to chronic mechanical allodynia after peripheral nerve injuries. However, it is still largely unknown where these T cells infiltrate along the somatosensory pathways transmitting mechanical allodynia to initiate the development of chronic mechanical allodynia after nerve injuries. Therefore, the purpose of this study was to ascertain the definite neuroimmune interface for these T cells to initiate the development of chronic mechanical allodynia after peripheral nerve injuries. Methods First, we utilized both chromogenic and fluorescent immunohistochemistry (IHC) to map αβ T cells along the somatosensory pathways for the transmission of mechanical allodynia after modified spared nerve injuries (mSNIs), i.e., tibial nerve injuries, in adult male Sprague-Dawley rats. We further characterized the molecular identity of these αβ T cells selectively infiltrating into the leptomeninges of L4 dorsal roots (DRs). Second, we identified the specific origins in Lumbar Lymph Nodes (LLNs) for CD4+ αβ T cells selectively present in the leptomeninges of L4 DRs by two experiments: (1) chromogenic IHC in these Lymph Nodes for CD4+ αβ T cell responses after mSNIs and (2) fluorescent IHC for temporal dynamics of CD4+ αβ T cell infiltration into the L4 DR leptomeninges after mSNIs in prior Lymphadenectomized or sham-operated animals to LLNs. Finally, following mSNIs, we evaluated the effects of region-specific targeting of these T cells through prior Lymphadenectomy to LLNs and chronic intrathecal application of the suppressive anti-αβTCR antibodies on the development of mechanical allodynia by von Frey hair test and spinal glial or neuronal activation by fluorescent IHC. Results Our results showed that during the sub-acute phase after mSNIs, αβ T cells selectively infiltrate into the leptomeninges of the Lumbar DRs along the somatosensory pathways responsible for transmitting mechanical allodynia. Almost all these αβ T cells are CD4 positive. Moreover, the temporal dynamics of CD4+ αβ T cell infiltration into the Lumbar DR leptomeninges are specifically determined by LLNs after mSNIs. Prior Lymphadenectomy to LLNs specifically reduces the development of mSNI-induced chronic mechanical allodynia. More importantly, intrathecal application of the suppressive anti-αβTCR antibodies reduces the development of mSNI-induced chronic mechanical allodynia. In addition, prior Lymphadenectomy to LLNs attenuates mSNI-induced spinal activation of glial cells and PKCγ+ excitatory interneurons. Conclusions The noteworthy results here provide the first evidence that CD4+ αβ T cells selectively infiltrate into the DR leptomeninges of the somatosensory pathways transmitting mechanical allodynia and contribute to the transition from acute to chronic mechanical allodynia after peripheral nerve injuries
You-quan Ding - One of the best experts on this subject based on the ideXlab platform.
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CD4+ αβ T cell infiltration into the leptomeninges of Lumbar dorsal roots contributes to the transition from acute to chronic mechanical allodynia after adult rat tibial nerve injuries.
Journal of neuroinflammation, 2018Co-Authors: You-quan Ding, Xia Xiao, Hong-yi RenAbstract:Antigen-specific and MHCII-restricted CD4+ αβ T cells have been shown or suggested to play an important role in the transition from acute to chronic mechanical allodynia after peripheral nerve injuries. However, it is still largely unknown where these T cells infiltrate along the somatosensory pathways transmitting mechanical allodynia to initiate the development of chronic mechanical allodynia after nerve injuries. Therefore, the purpose of this study was to ascertain the definite neuroimmune interface for these T cells to initiate the development of chronic mechanical allodynia after peripheral nerve injuries. First, we utilized both chromogenic and fluorescent immunohistochemistry (IHC) to map αβ T cells along the somatosensory pathways for the transmission of mechanical allodynia after modified spared nerve injuries (mSNIs), i.e., tibial nerve injuries, in adult male Sprague-Dawley rats. We further characterized the molecular identity of these αβ T cells selectively infiltrating into the leptomeninges of L4 dorsal roots (DRs). Second, we identified the specific origins in Lumbar Lymph Nodes (LLNs) for CD4+ αβ T cells selectively present in the leptomeninges of L4 DRs by two experiments: (1) chromogenic IHC in these Lymph Nodes for CD4+ αβ T cell responses after mSNIs and (2) fluorescent IHC for temporal dynamics of CD4+ αβ T cell infiltration into the L4 DR leptomeninges after mSNIs in prior Lymphadenectomized or sham-operated animals to LLNs. Finally, following mSNIs, we evaluated the effects of region-specific targeting of these T cells through prior Lymphadenectomy to LLNs and chronic intrathecal application of the suppressive anti-αβTCR antibodies on the development of mechanical allodynia by von Frey hair test and spinal glial or neuronal activation by fluorescent IHC. Our results showed that during the sub-acute phase after mSNIs, αβ T cells selectively infiltrate into the leptomeninges of the Lumbar DRs along the somatosensory pathways responsible for transmitting mechanical allodynia. Almost all these αβ T cells are CD4 positive. Moreover, the temporal dynamics of CD4+ αβ T cell infiltration into the Lumbar DR leptomeninges are specifically determined by LLNs after mSNIs. Prior Lymphadenectomy to LLNs specifically reduces the development of mSNI-induced chronic mechanical allodynia. More importantly, intrathecal application of the suppressive anti-αβTCR antibodies reduces the development of mSNI-induced chronic mechanical allodynia. In addition, prior Lymphadenectomy to LLNs attenuates mSNI-induced spinal activation of glial cells and PKCγ+ excitatory interneurons. The noteworthy results here provide the first evidence that CD4+ αβ T cells selectively infiltrate into the DR leptomeninges of the somatosensory pathways transmitting mechanical allodynia and contribute to the transition from acute to chronic mechanical allodynia after peripheral nerve injuries.
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CD4+ αβ T cell infiltration into the leptomeninges of Lumbar dorsal roots contributes to the transition from acute to chronic mechanical allodynia after adult rat tibial nerve injuries
BMC, 2018Co-Authors: You-quan Ding, Xia Xiao, Hong-yi RenAbstract:Abstract Background Antigen-specific and MHCII-restricted CD4+ αβ T cells have been shown or suggested to play an important role in the transition from acute to chronic mechanical allodynia after peripheral nerve injuries. However, it is still largely unknown where these T cells infiltrate along the somatosensory pathways transmitting mechanical allodynia to initiate the development of chronic mechanical allodynia after nerve injuries. Therefore, the purpose of this study was to ascertain the definite neuroimmune interface for these T cells to initiate the development of chronic mechanical allodynia after peripheral nerve injuries. Methods First, we utilized both chromogenic and fluorescent immunohistochemistry (IHC) to map αβ T cells along the somatosensory pathways for the transmission of mechanical allodynia after modified spared nerve injuries (mSNIs), i.e., tibial nerve injuries, in adult male Sprague-Dawley rats. We further characterized the molecular identity of these αβ T cells selectively infiltrating into the leptomeninges of L4 dorsal roots (DRs). Second, we identified the specific origins in Lumbar Lymph Nodes (LLNs) for CD4+ αβ T cells selectively present in the leptomeninges of L4 DRs by two experiments: (1) chromogenic IHC in these Lymph Nodes for CD4+ αβ T cell responses after mSNIs and (2) fluorescent IHC for temporal dynamics of CD4+ αβ T cell infiltration into the L4 DR leptomeninges after mSNIs in prior Lymphadenectomized or sham-operated animals to LLNs. Finally, following mSNIs, we evaluated the effects of region-specific targeting of these T cells through prior Lymphadenectomy to LLNs and chronic intrathecal application of the suppressive anti-αβTCR antibodies on the development of mechanical allodynia by von Frey hair test and spinal glial or neuronal activation by fluorescent IHC. Results Our results showed that during the sub-acute phase after mSNIs, αβ T cells selectively infiltrate into the leptomeninges of the Lumbar DRs along the somatosensory pathways responsible for transmitting mechanical allodynia. Almost all these αβ T cells are CD4 positive. Moreover, the temporal dynamics of CD4+ αβ T cell infiltration into the Lumbar DR leptomeninges are specifically determined by LLNs after mSNIs. Prior Lymphadenectomy to LLNs specifically reduces the development of mSNI-induced chronic mechanical allodynia. More importantly, intrathecal application of the suppressive anti-αβTCR antibodies reduces the development of mSNI-induced chronic mechanical allodynia. In addition, prior Lymphadenectomy to LLNs attenuates mSNI-induced spinal activation of glial cells and PKCγ+ excitatory interneurons. Conclusions The noteworthy results here provide the first evidence that CD4+ αβ T cells selectively infiltrate into the DR leptomeninges of the somatosensory pathways transmitting mechanical allodynia and contribute to the transition from acute to chronic mechanical allodynia after peripheral nerve injuries
Ling Cao - One of the best experts on this subject based on the ideXlab platform.
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CNS‐infiltrating CD4+ T Lymphocytes contribute to murine spinal nerve transection‐induced neuropathic pain
European journal of immunology, 2008Co-Authors: Ling Cao, Joyce A DeleoAbstract:We previously reported leukocytic infiltration into the Lumbar spinal cord in a rodent spinal nerve L5 transection (L5Tx) neuropathic pain model. Here, we further investigated the role of infiltrating T Lymphocytes in the etiology of persistent pain following L5Tx. T Lymphocyte-deficient nude mice showed no evident mechanical hypersensitivity after day 3 of L5Tx compared to wild-type BALB/c mice. Through FACS analysis, we determined that significant leukocytic infiltration (CD45(hi)) into the Lumbar spinal cord peaked at day 7 post L5Tx. These infiltrating leukocytes contained predominantly CD4(+) but not CD8(+) T Lymphocytes. B Lymphocytes, natural killer cells and macrophages were not detected at day 7 post L5Tx. No differences in the activation of peripheral CD4(+) T Lymphocytes were detected in either the spleen or Lumbar Lymph Nodes between L5Tx and sham surgery groups. Further, CD4 KO mice displayed significantly decreased mechanical hypersensitivity after day 7 of L5Tx, and adoptive transfer of CD4(+) leukocytes reversed this effect. Decreased immunoreactivity of glial fibrillary acidic protein observed in CD4 KO mice post L5Tx indicated possible T Lymphocyte-glial interactions. These results strongly support a contributing role of spinal cord-infiltrating CD4(+) T Lymphocytes versus peripheral CD4(+) T Lymphocytes in the maintenance of nerve injury-induced neuropathic pain.
M Torii - One of the best experts on this subject based on the ideXlab platform.
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BRIEF COMMUNICATION Peripheral Neuroblastoma in a Young Beagle Dog*
2016Co-Authors: S Matsushima, T Maruyama, M ToriiAbstract:shionogi.co.jp. A peripheral neuroblastoma was found in the abdominal cavity of a young male beagle dog. The large tumor mass involved the left kidney and both adrenal glands. Histologically, a major portion of the neoplasm consisted of lobulated sheets of small round cells with hyperchromatic nuclei mixed with polygonal cells and neuropil. Small clusters of polygonal cells with abundant eosinophilic cytoplasm and a trabecular growth pattern were observed adjacent to some of the tumor lobules. Small, round neoplastic cells metastasized to Lumbar Lymph Nodes and also to the adrenal glands. The neoplastic cells were positive for neuron-specific enolase, synaptophysin, and neurofilament protein. Electron micrographs revealed intracytoplasmic dense core granules, microtubules, inter-mediate filaments, and desmosomes in the cytoplasm of the neoplastic cells. Keywords. Neoplasia; immunohistochemistry; ultrastructure; abdominal cavity Neuroblastoma, one of the most common neoplasms in human infancy and childhood, is thought to be derived from primordial neural crest cells migrating from the mantle layer of the developing spinal cord. During de-velopment, neural crest cells populate the primordium o
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Peripheral Neuroblastoma in a Young Beagle Dog
Toxicologic pathology, 1998Co-Authors: S Matsushima, T Maruyama, M ToriiAbstract:A peripheral neuroblastoma was found in the abdominal cavity of a young male beagle dog. The large tumor mass involved the left kidney and both adrenal glands. Histologically, a major portion of the neoplasm consisted of lobulated sheets of small round cells with hyperchromatic nuclei mixed with polygonal cells and neuropil. Small clusters of polygonal cells with abundant eosinophilic cytoplasm and a trabecular growth pattern were observed adjacent to some of the tumor lobules. Small, round neoplastic cells metastasized to Lumbar Lymph Nodes and also to the adrenal glands. The neoplastic cells were positive for neuron-specific enolase, synaptophysin, and neurofilament protein. Electron micrographs revealed intracytoplasmic dense core granules, microtubules, intermediate filaments, and desmosomes in the cytoplasm of the neoplastic cells.
