Diet and multiple sclerosis

Lauer, Klaus

doi:10.1212/wnl.49.2_suppl_2.s55

Cited by 81 publications

(56 citation statements)

References 16 publications

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“…In fact, chance may play a major role in determining whether or not molecular mimicry between MOG and BTN leads to a detrimental or protective immune response in any particular individual. Intriguingly, epidemiological studies associate the prevalence of MS with the consumption of milk and dairy produce (41,42,43), but whether this is related to molecular mimicry involving MOG and BTN remains a matter of speculation. Table I.…”

Section: Discussionmentioning

confidence: 99%

“…Epidemiological studies repeatedly associate the prevalence of MS with dietary factors including the consumption of milk and dairy produce (41)(42)(43), and this has lead to speculation that molecular mimicry involving BTN may modulate MOG-specific autoimmune responses in humans (19,44). To examine this possible link in more detail, we investigated the Ab response to MOG Igd in patients with MS for evidence of molecular mimicry with BTN.…”

mentioning

confidence: 99%

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Antibody Cross-Reactivity between Myelin Oligodendrocyte Glycoprotein and the Milk Protein Butyrophilin in Multiple Sclerosis

Guggenmos

Schubart

Ogg

et al. 2004

The Journal of Immunology

119

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The etiology of multiple sclerosis (MS) is believed to involve environmental factors, but their identity and mode of action are unknown. In this study, we demonstrate that Ab specific for the extracellular Ig-like domain of myelin oligodendrocyte glycoprotein (MOG) cross-reacts with a homologous N-terminal domain of the bovine milk protein butyrophilin (BTN). Analysis of paired samples of MS sera and cerebrospinal fluid (CSF) identified a BTN-specific Ab response in the CNS that differed in its epitope specificity from that in the periphery. This effect was statistically significant for the Ab response to BTN76–100 (p = 0.0026), which cosequestered in the CSF compartment with Ab to the homologous MOG peptide MOG76–100 in 34% of MS patients (n = 35). These observations suggested that intratheccal synthesis of Ab recognizing BTN peptide epitopes in the CNS was sustained by molecular mimicry with MOG. Formal evidence of molecular mimicry between the two proteins was obtained by analyzing MOG-specific autoantibodies immunopurified from MS sera. The MOG-specific Ab repertoire cross-reacts with multiple BTN peptide epitopes including a MOG/BTN76–100-specific component that occurred at a higher frequency in MS patients than in seropositive healthy controls, as well as responses to epitopes within MOG/BTN1–39 that occur at similar frequencies in both groups. The demonstration of molecular mimicry between MOG and BTN, along with sequestration of BTN-reactive Ab in CSF suggests that exposure to this common dietary Ag may influence the composition and function of the MOG-specific autoimmune repertoire during the course of MS.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Antibody Cross-Reactivity between Myelin Oligodendrocyte Glycoprotein and the Milk Protein Butyrophilin in Multiple Sclerosis

Guggenmos

Schubart

Ogg

et al. 2004

The Journal of Immunology

119

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“…However, no virus has yet been identified that causes MS (Genain & Hauser, 1997;Monteyne et al, 1998). Other environmental factors, possibly contributing to susceptibility for MS, are sunlight and nutrition (Agranoff & Goldberg, 1974;Alter et al, 1974;Goldberg, 1974a, b;Murrell et al, 1991;Esparza et al, 1995;Hutter & Laing, 1996;Hayes et al, 1997;Lauer, 1997;Van Noort & Amor, 1998). The vast amount of literature on nutrition and MS indicates that food intake may be an influencing factor determining the disease susceptibility.…”

Section: Etiological Factors Of Msmentioning

confidence: 99%

Multiple sclerosis and vitamin D: an update

et al. 2004

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MS is a chronic, immune-mediated inflammatory and neurodegenerative disease of the central nervous system (CNS), with an etiology that is not yet fully understood. The prevalence of MS is highest where environmental supplies of vitamin D are lowest. It is well recognized that the active hormonal form of vitamin D, 1,25-dihydroxyvitamin D (1,25-(OH) 2 D), is a natural immunoregulator with anti-inflammatory action. The mechanism by which vitamin D nutrition is thought to influence MS involves paracrine or autocrine metabolism of 25OHD by cells expressing the enzyme 1a-OHase in peripheral tissues involved in immune and neural function. Administration of the active metabolite 1,25-(OH) 2 D in mice and rats with experimental allergic encephalomyelitis (EAE, an animal model of MS) not only prevented, but also reduced disease activity. 1,25-(OH) 2 D alters dendritic cell and T-cell function and regulates macrophages in EAE. Interestingly, 1,25-(OH) 2 D is thought to be operating on CNS constituent cells as well. Vitamin D deficiency is caused by insufficient sunlight exposure or low dietary vitamin D 3 intake. Subtle defects in vitamin D metabolism, including genetic polymorphisms related to vitamin D, might possibly be involved as well. Optimal 25OHD serum concentrations, throughout the year, may be beneficial for patients with MS, both to obtain immune-mediated suppression of disease activity, and also to decrease disease-related complications, including increased bone resorption, fractures, and muscle weakness.

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“…7-9), but the issue is not settled in either disease (10). In addition, epidemiological surveys identified nutritional elements as risk factors for the development of autoimmunity, specifically linking high exposure to cow milk protein (CMP) with the risk to develop MS (11)(12)(13)(14) or autoimmune diabetes, where the available literature is more recent and more extensive (reviewed in Refs. [15][16][17].…”

Section: Ultiple Sclerosis (Ms)mentioning

confidence: 99%

T Cells of Multiple Sclerosis Patients Target a Common Environmental Peptide that Causes Encephalitis in Mice

Winer

Astsaturov

Cheung

et al. 2001

The Journal of Immunology

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Multiple sclerosis (MS) is a chronic autoimmune disease triggered by unknown environmental factors in genetically susceptible hosts. MS risk was linked to high rates of cow milk protein (CMP) consumption, reminiscent of a similar association in autoimmune diabetes. A recent rodent study showed that immune responses to the CMP, butyrophilin, can lead to encephalitis through antigenic mimicry with myelin oligodendrocyte glycoprotein. In this study, we show abnormal T cell immunity to several other CMPs in MS patients comparable to that in diabetics. Limited epitope mapping with the milk protein BSA identified one specific epitope, BSA193, which was targeted by most MS but not diabetes patients. BSA193 was encephalitogenic in SJL/J mice subjected to a standard protocol for the induction of experimental autoimmune encephalitis. These data extend the possible, immunological basis for the association of MS risk, CMP, and CNS autoimmunity. To pinpoint the same peptide, BSA193, in encephalitis-prone humans and rodents may imply a common endogenous ligand, targeted through antigenic mimicry.

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Diet and multiple sclerosis

Cited by 81 publications

References 16 publications

Antibody Cross-Reactivity between Myelin Oligodendrocyte Glycoprotein and the Milk Protein Butyrophilin in Multiple Sclerosis

Antibody Cross-Reactivity between Myelin Oligodendrocyte Glycoprotein and the Milk Protein Butyrophilin in Multiple Sclerosis

Multiple sclerosis and vitamin D: an update

T Cells of Multiple Sclerosis Patients Target a Common Environmental Peptide that Causes Encephalitis in Mice

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