паранеопластический энцефалит, ассоциированный с антителами к белкам нейрональной мембраны

Примерно так это будет выглядеть описательно.

Индуцированный можно заменить на "обусловленный", "опосредованный".

По желанию можно более подробно описать "HuD" как "антиген HuD"

Механизм аналогичен этому.

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Note added at 42 mins (2017-01-06 12:55:18 GMT)
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Anti-Hu (antineuronal nuclear antibody 1; ANNA1) and anti-Ri (antineuronal nuclear antibody 2; ANNA2) antibodies are paraneoplastic autoantibodies which react with nuclear and cytoplasmic proteins of neurons throughout the central nervous system. Anti-Hu antibody is closely associated with small cell carcinoma of the lung and has been reported in patients with a wide spectrum of paraneoplastic neurological disorders, including limbic encephalitis, cerebellar degeneration, brainstem encephalitis, dorsal sensory neuronopathy, motor neuron disease, and gastroparesis [1,2]. Anti-Ri antibody, found predominantly in patients with breast adenocarcinomas and small cell carcinoma of the lung, has been associated with syndromes of opsoclonus/ataxia, cerebellar degeneration, limbic or brainstem encephalitis, ophthalmoplegia, laryngeal dystonia, and gastroparesis [3–12].

Our study demonstrated that two major paraneoplastic autoantibodies, anti-Hu and anti-Ri, were both taken up by neurons throughout both hippocampus and cerebellum, and that anti-Hu antibody caused neuronal death whereas anti-Ri antibody did not affect neuronal survival. Neuronal death produced by anti-Hu antibody involved binding to the intracellular Hu antigen and occurred in the absence of T cells or Fc receptor-positive immune cells, suggesting that this antibody-antigen interaction may be directly responsible for paraneoplastic neuronal death. The lack of cytotoxic effect seen in cultures incubated with anti-Ri antibody raises questions as to whether anti-Ri antibody, unlike anti-Hu antibody, might impair neuronal function without producing cell death. The ability of antibodies to enter neurons and bind to intracellular antigens may play a key role in human paraneoplastic neurological disease and could be involved in other autoimmune or infectious central nervous system disorders.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4174281/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3913668/

https://www.ncbi.nlm.nih.gov/pubmed/12851872

The search for the molecular targets of anti-Hu antibodies led to the identification of 3 proteins of approximate molecular weight of 35–38 KDa expressed in the CNS. In malignant cells, the 38 KDa band is not detected. Screening a cDNA expression library from the human cerebellum with the sera of patients affected by the anti-Hu syndrome allowed for the cloning of the highly homologous genes HuD (official name: ELAV like neuron-specific RNA binding protein 4, ELAVL4), HuC, (official name: ELAV like neuron-specific RNA binding protein 3, ELAVL3) and HuB (official name; ELAV like neuron-specific RNA binding protein 2, ELAVL2; also known as Hel-N1). The Hu family actually consists of 4 members: HuA (official name: ELAV like RNA binding protein 1, ELAVL1; also known as HuR), HuB, HuC, and HuD. These proteins share extensive homology and are highly-conserved across species.13 HuA, the most divergent, is ubiquitously expressed13,14 and is not recognized by paraneoplastic antibodies. In contrast, HuB, HuC, and HuD expression is restricted to neurons, which all express one or more of these proteins.13

Whereas HuB, HuC, and HuD are all expressed in CNS neurons, HuD is Hu antigen most frequently expressed by SCLC cells. This is a consistent observation in SCLC patients, irrespective of whether they develop PEM/PSN or not.6,25 The HuD-coding mRNA has also been detected in SCLC cell lines.26 No somatic mutations or deletions/insertions affecting HuD have been observed in SCLC cell lines or tumors, including those from patients with PEM/PSN.27-29 However, a fine analysis of the post-translational modifications of HuD in cancer cells from patients developing or not PNDs has not been performed to date. Indeed, malignant cell-specific post-translational modifications of HuD may favor the development of an immune response that cross-reacts with neuronal Hu proteins. Moreover, the possible function(s) of HuD in the tumor biology, if any, has not been uncovered so far. SCLC and many cancers associated with PEM/PSN exhibit a neuroectodermal origin. The neuroectoderm includes the neural crest (melanocytes, dorsal root ganglia, ganglia of the autonomous nervous system, adrenal glands, Schwann cells, …) and the neural tube (brain, spinal cord, retina, neurohypophysis). As a result, most SCLCs are composed of cells with a neuroendocrine phenotype, characterized by elevated expression levels of L-dopa decarboxylase, neuron-specific enolase, and neuropeptides.30 These features resemble those of neural crest-derived endocrine cells disseminated in the normal bronchial mucosa. Such a shared embryonic origin could explain the expression of HuD by SCLC cells.

Functional properties of anti-Hu antibodies

Since anti-Hu antibodies target intracellular antigens, their pathogenic and antitumor potential is questionable. Interestingly, a study documented the expression of Hu-related antigens on the surface of SCLC and neuroblastoma cell lines.45 Whether neurons exhibit a similar expression pattern of Hu proteins is currently undetermined.

Experimentally, the contribution of anti-Hu antibodies to the development of PEM/PSN has been investigated in vitro, in cell cultures, and in vivo, upon injection of human antibodies to laboratory animals. In vitro, monoclonal antibodies specific for HuD have been shown to promote the apoptotic demise of neuroblastoma cell lines and primary myenteric neurons.46 The serum or IgG preparations from patients with the anti-Hu syndrome could also kill human HuD-expressing cell lines and primary rodent neurons, a phenomenon that was accelerated in the presence of the complement system.46-48 However, this observation is not universal, and the lack of cytotoxic effects of anti-Hu positive sera on HuD+ cancer cells or primary murine neurons has also been reported.49,50 Moreover, even when neuronal cytotoxicity was observed, the specificity of the pathogenic autoantibodies was questioned, as the patients’ IgGs, but not an anti-HuD monoclonal antibody tested alongside, mediated such an effect.48 As discussed above, the serum of patients with PND often contain multiple neuron-targeting autoantibodies, some of which recognize surface receptors. Therefore, unless proper specificity assays are conducted, for instance upon pre-absorbing IgG preparations on recombinant HuD, formal conclusions regarding the impact of anti-Hu antibodies on neuronal viability are difficult to reach.

The intravenous administration of IgGs from patients with PEM/PSN and high titers of anti-Hu antibody to mice did not result in any CNS lesion.51,52 In addition, all attempts to generate rodent models of the anti-Hu syndrome upon immunization with recombinant HuD failed to induce any signs of disease, CNS inflammation or neuronal degeneration, despite the development of high circulating titers of anti-HuD antibodies.51,53

Thus, although the presence of high anti-Hu titers in PND patients represents a highly valuable diagnostic tool, their role in disease pathogenesis appears at best dubious. Nevertheless, these autoantibodies reflect a strong autoimmune/antitumor immune response in which autoreactive T cells, specific for HuD or other self antigens, are likely to be involved.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3913668/