Sural nerve T-cell receptor Vβ gene utilization in chronic inflammatory demyelinating polyneuropathy and vasculitic neuropathy

Bosboom, W. M. J.; Berg, Leonard H van den; Mollee, I.; Sasker, L.D.; Jansen, Jenny; Wokke, John H. J.; Logtenberg, Ton

doi:10.1212/wnl.56.1.74

Cited by 39 publications

(13 citation statements)

References 37 publications

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“…It is important to note that using a four-color flow cytometer, the IOTest Beta Mark 1 kit and the anti-Vb6.7 mAb, it was possible to determine the distribution of 25 Vb families in only nine test tubes, for both CD41 and CD81 subsets, and to make results available on the same day the lymph node was excised. These mAbs have also been used to study T-cell Vb families by immunohistohistology on biopsies (3,17,33,40); however, the analysis was hardly reproducible or precise. Alternative techniques for TCR diversity exploration imply molecular approaches.…”

Section: Discussionmentioning

confidence: 99%

Efficient characterization of the TCR repertoire in lymph nodes by flow cytometry

et al. 2009

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Analysis of the T-cell receptor (TCR) repertoire by flow cytometry proved to be relevant for investigating T-cell diversity and detecting reactive cells in blood samples. We used this approach to characterize non-malignant T-lymphocytes in lymph nodes and give insights into their origin. The TCR repertoire of CD41 and CD81 T-cells from 81 lymph nodes was analyzed with a four-color flow cytometer using a wide panel of 25 anti-Vb monoclonal antibodies. Flow cytometry proved to be a useful and informative technique. We demonstrated a diversified TCR-Vb repertoire, and only low level expansions, in 53% of the samples. They involved nearly all Vb families, were more frequent in the CD81 subset of older patients, but were not related to pathology. No evidence could be demonstrated in favor of stimulation by common antigens. Interestingly, the TCR-Vb repertoire proved to be very similar in lymph nodes and blood samples. Our results argue that in the cases studied, lymph node enlargement is mainly due to an increased homing of circulating T-cells. They also provide reference values for expression of 25 TCR-Vb in lymph nodes, which could serve as a basis for further applications in diagnosis of T-cell lymphoproliferative disorders. ' 2009 International Society for Advancement of Cytometry

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Section: Discussionmentioning

confidence: 99%

Efficient characterization of the TCR repertoire in lymph nodes by flow cytometry

et al. 2009

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“…If antigen-specific T cells were being actively recruited into the nerve by an immune stimulus and/or proliferating there in response to a local immune stimulus (i.e., clonal expansion), one would expect that many of the T cells present in the biopsy would express receptors for the same epitopes. Since they do not (25), the more likely explana-tion of increased T lymphocytes in the region rests simply on blood-nerve barrier breakdown.…”

Section: C) Evidence For Ischemia-induced Nerve and Immune Changesmentioning

confidence: 99%

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

Watkins

Maier

2002

Physiological Reviews

650

433

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Chronic pain can occur after peripheral nerve injury, infection, or inflammation. Under such neuropathic pain conditions, sensory processing in the affected body region becomes grossly abnormal. Despite decades of research, currently available drugs largely fail to control such pain. This review explores the possibility that the reason for this failure lies in the fact that such drugs were designed to target neurons rather than immune or glial cells. It describes how immune cells are a natural and inextricable part of skin, peripheral nerves, dorsal root ganglia, and spinal cord. It then examines how immune and glial activation may participate in the etiology and symptomatology of diverse pathological pain states in both humans and laboratory animals. Of the variety of substances released by activated immune and glial cells, proinflammatory cytokines (tumor necrosis factor, interleukin-1, interleukin-6) appear to be of special importance in the creation of peripheral nerve and neuronal hyperexcitability. Although this review focuses on immune modulation of pain, the implications are pervasive. Indeed, all nerves and neurons regardless of modality or function are likely affected by immune and glial activation in the ways described for pain.

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“…Apparently, the T-cell populations are heterogeneous and belong to both the CD4 and CD8 subgroups and carry the ab or the gd T-cell receptor [20][21][22][23][24]. In order to generate inflammatory lesions in the peripheral nerve, activated T cells need to cross the BNB.…”

Section: T Lymphocytes In the Peripheral Nervementioning

confidence: 99%

Immune circuitry in the peripheral nervous system

Kieseier

Hartung

Wiendl

2006

Current Opinion in Neurology

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The application of innovative and cutting-edge technologies to the study of immunoinflammatory disorders of the peripheral nervous system provides a better understanding of underlying principles of the organization of the immune network present in the peripheral nerve and its dialogue with the systemic immune system. This may foster the development of specific and highly effective therapies for immune-mediated disorders of the peripheral nerve.

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Sural nerve T-cell receptor Vβ gene utilization in chronic inflammatory demyelinating polyneuropathy and vasculitic neuropathy

Cited by 39 publications

References 37 publications

Efficient characterization of the TCR repertoire in lymph nodes by flow cytometry

Efficient characterization of the TCR repertoire in lymph nodes by flow cytometry

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

Immune circuitry in the peripheral nervous system

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