Enolase autoantibodies and retinal function in multiple sclerosis patients

Forooghian, Farzin; Adamus, Grażyna; Sproule, Melanie; Westall, Carol A.; O’Connor, Paul

doi:10.1007/s00417-006-0527-8

Cited by 27 publications

(24 citation statements)

References 52 publications

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“…We, and others have reported the presence of anti-NNE antibodies in association with retinopathy in MS patients (11,12). Furthermore, we have reported an increased prevalence of enolase autoantibodies in MS patients compared to healthy controls (13). Neuron-specific enolase (NSE) is the enolase isoform found in the CNS.…”

Section: Introductionmentioning

confidence: 82%

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

et al. 2007

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Introduction-Although myelin autoimmunity is known to be a major factor in the pathogenesis of multiple sclerosis (MS), the role of nonmyelin antigens is less clear. Given the complexity of this disease, it is possible that autoimmunity against nonmyelin antigens also has a pathogenic role. Autoantibodies against enolase and arrestin have previously been reported in MS patients. The Tcell response to these antigens, however, has not been established.

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Section: Introductionmentioning

confidence: 82%

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

et al. 2007

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“…18 PDAC patients did not display signs of autoimmunity, though the presence of anti-a-enolase antibodies has been described in patients with autoimmune disorders. 23,[34][35][36][37][38][39] It is known that a-enolase expressed at cell surface acts as a plasminogen receptor. 28,40 The bound plasminogen is more efficiently activated to plasmin and thus contributes to pathological processes such as tumor cell invasion, metastases and inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

An integrated humoral and cellular response is elicited in pancreatic cancer by α‐enolase, a novel pancreatic ductal adenocarcinoma‐associated antigen

Cappello¹,

Tomaino²,

Chiarle³

et al. 2009

Intl Journal of Cancer

108

125

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Pancreatic ductal adenocarcinoma (PDAC) is a fatal disease with a very poor 5-year survival rate. a-Enolase is a glycolytic enzyme that also acts as a surface plasminogen receptor. We find that it is overexpressed in PDAC and present on the cell surface of PDAC cell lines. The clinical correlation of its expression with tumor status has been reported for lung and hepatocellular carcinoma. We have previously demonstrated that sera from PDAC patients contain IgG autoantibodies to a-enolase. The present work was intended to assess the ability of a-enolase to induce antigen-specific T cell responses. We show that a-enolase-pulsed dendritic cells (DC) specifically stimulate healthy autologous T cells to proliferate, secrete IFN-c and lyse PDAC cells but not normal cells. In vivo, a-enolase-specific T cells inhibited the growth of PDAC cells in immunodeficient mice. In 8 out of 12 PDAC patients with circulating IgG to a-enolase, the existence of a-enolase-specific T cells was also demonstrated. Taken as a whole, these results indicate that a-enolase elicits a PDAC-specific, integrated humoral and cellular response. It is thus a promising and clinically relevant molecular target candidate for immunotherapeutic approaches as new adjuvants to conventional treatments in pancreatic cancer. ' 2009 UICC

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“…For example, whereas we have identified aldolase A, (another glycolytic enzyme) as a potential target, immunization of C57BL/6 and NOD mice or Lewis rats with this protein does not lead to the development of any diseases (59). Likewise, whereas antibodies to alpha-enolase are associated with autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus and mixed cryoglobulnemia, these are nonpathogenic (45).…”

Section: Discussionmentioning

confidence: 99%

“…The molecule of neuronal origin, ␥ enolase, is generally found elevated in CSF of patients with neurodegenerative disorders (45) and is involved in actin filament disassembly. Notably, we detected ␣␤-crystallin, a molecule present at enhanced levels in oligodendrocytes and astrocytes in MS lesions.…”

Section: Fig 2 Representative Two-dimensional Blot Showing the Reacmentioning

confidence: 99%

A Novel Unbiased Proteomic Approach to Detect the Reactivity of Cerebrospinal Fluid in Neurological Diseases

Menon

Steer

Short

et al. 2011

Molecular & Cellular Proteomics

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Neurodegenerative diseases, such as multiple sclerosis represent global health issues. Accordingly, there is an urgent need to understand the pathogenesis of this and other central nervous system disorders, so that more effective therapeutics can be developed. Cerebrospinal fluid is a potential source of important reporter molecules released from various cell types as a result of central nervous system pathology. Here, we report the development of an unbiased approach for the detection of reactive cerebrospinal fluid molecules and target brain proteins from patients with multiple sclerosis. To help identify molecules that may serve as clinical biomarkers for multiple sclerosis, we have biotinylated proteins present in the cerebrospinal fluid and tested their reactivity against brain homogenate as well as myelin and myelin-axolemmal complexes. Proteins were separated by two-dimensional gel electrophoresis, blotted onto membranes and probed separately with biotinylated unprocessed cerebrospinal fluid samples. Protein spots that reacted to two or more multiple sclerosis-cerebrospinal fluids were further analyzed by matrix assisted laser desorption ionization-time-of-flight time-of-flight mass spectrometry. In addition to previously reported proteins found in multiple sclerosis cerebrospinal fluid, such as ␣␤ crystallin, enolase, and 14 -3-3-protein, we have identified several additional molecules involved in mitochondrial and energy metabolism, myelin gene expression and/or cytoskeletal organization. These include aspartate aminotransferase, cyclophilin-A, quaking protein, collapsin response mediator protein-2, ubiquitin carboxy-terminal hydrolase L1, and cofilin. To further validate these findings, the cellular expression pattern of collapsin response mediator protein-2 and ubiquitin carboxy-terminal hydrolase L1 were investigated in human chronic-active MS lesions by immunohistochemistry. The observation that in multiple sclerosis lesions phosphorylated collapsin response mediator protein-2 was increased, whereas Ubiquitin carboxy-terminal hydrolase L1 was down-regulated, not only highlights the importance of these molecules in the pathology of this disease, but also illustrates the use of our approach in attempting to decipher the complex pathological processes leading to multiple sclerosis and other neurodegenerative diseases.

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Enolase autoantibodies and retinal function in multiple sclerosis patients

Cited by 27 publications

References 52 publications

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

An integrated humoral and cellular response is elicited in pancreatic cancer by α‐enolase, a novel pancreatic ductal adenocarcinoma‐associated antigen

A Novel Unbiased Proteomic Approach to Detect the Reactivity of Cerebrospinal Fluid in Neurological Diseases

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