Research paperSynergy between antibody and P2-reactive T cells in experimental allergic neuritis
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2020, Journal of NeuroimmunologyCitation Excerpt :EAN is an autoimmune disease mainly mediated by T cells, that can transfer disease (Hughes et al., 1981) and mediate demyelination when injected into peripheral nerves (Hodgkinson et al., 1994). Others have shown a role for antibody mediating injury either alone (Harvey and Pollard, 1992) or with T cells to break down the blood nerve barrier (Spies et al., 1995). In both T cell and antibody responses, CD4+T cells are central to activation of the effector mechanisms.
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2019, The Autoimmune DiseasesPeripheral Neuropathies
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2013, Journal of the Neurological SciencesCitation Excerpt :In chronic cases well developed onion bulb formation may be seen. Inflammatory cells, CD4 and CD8 T cells and macrophages may be seen within the endoneurium, in perivascular regions and associated response is associated with upregulation of MHC molecules on Schwann cells [8] and increased permeability of the blood nerve barrier as shown by experimental studies [9,10]. Both T and B lymphocytes have been shown within the nerve lesions of CIDP [8,11] and macrophages clearly play a prime role in myelin phagocytosis [12,13].
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2012, American Journal of PathologyCitation Excerpt :The reasons why immunization toward NF186 did not generate significant neurologic signs in Lewis rats are unclear. Several previous studies documented that anti-myelin antibodies necessitate T-cell response to pass the blood barrier in the peripheral nervous system and central nervous system.42,43 I demonstrate that anti-gliomedin IgG did not lead to a significant neuropathy in absence of blood-nerve barrier breakdown, emphasizing that EAN neuropathy is not solely humorally mediated but also implicating cellular factors that help antibodies gaining access to their targets.
IL-5 promotes induction of antigen-specific CD4<sup>+</sup>CD25<sup>+</sup> T regulatory cells that suppress autoimmunity
2012, BloodCitation Excerpt :rIL-5 treatment had no effect on anti-PNM Ab titers nor did it induce an IgG isotype shift to a Th2 type with more IgG1 and less complement-fixing IgG2 isotypes (Figure 4). Anti-PNM Abs have been implicated as mediators of demyelination in EAN31; however, activation of the membrane attack complex of complement is not essential for demyelination in EAN.19 Because there was no alteration in anti-PNM Ab titers or Ab isotype, the effect of rIL-5 on B cells in the lymph node at the site of immunization was not the explanation for its effects on EAN.