milchlos.de
milchlos.de
Seit neuestem wird MS mit Diabetes und Milch in Zusammenhang gebracht.
Kanadische Forscher sind im Jahre 2001 - bislang unwidersprochen - mit Studienergebnissen an die Öffentlichkeit getreten, die darlegen, dass Typ I Diabetes und MS immunologisch sehr ähnliche Erkrankungen sind, kaum voneinander unterscheidbar. Bei beiden Erkrankungen erstreckt sich die Autoimmunreaktion sowohl auf die Bauchspeicheldrüse, wie auf das bei MS betroffene Nervengewebe. Und in beiden Fällen sind Immunreaktionen auf Kuhmilchproteine involviert.
MS ist hauptsächlich auf Industrieländer, also die Milchländer beschränkt. Offenbar gibt es eine Verbindung zum Milchkonsum, bzw. zum Konsum von Milcheiweiß. Wer sich mit dem möglichen Ernährungsbezug von MS beschäftigen will, dem sei der eindrucksvolle Aufsatz zu MS und sie beeinflussende Umweltfaktoren wie Ernährung, u.a. tierische Eiweiße, Hefe und Leguminosen, des Kanadiers und Geologen Ashton F. Embry, übersetzt von Detlef Neumann empfohlen.
Aus Medline die Kurzfassung der kannadischen Studien:
J Immunol 2001 Feb 15;166(4):2831-41
Type I diabetes and multiple sclerosis patients target Islet plus central nervous system autoantigens; nonimmunized nonobese diabetic mice can develop autoimmune encephalitis.
Winer S, Astsaturov I, Cheung R, Gunaratnam L, Kubiak V, Cortez MA, Moscarello M, O'Connor PW, McKerlie C, Becker DJ, Dosch HM The Hospital For Sick Children, St. Michael's Hospital University of Toronto, Sunnybrook and Women's College Health Sciences Center University of Toronto, Ontario, Canada.
Type I diabetes and multiple sclerosis (MS) are distinct autoimmune diseases where T cells target either islet or CNS self-proteins. Unexpectedly, we found that autoreactive T cells in diabetic patients, relatives with high diabetes risk, nonobese diabetic (NOD) mice, and MS patients routinely target classical islet as well as CNS autoantigens. The pathogenic potential of CNS autoreactivity was testable in NOD mice. Pertussis holotoxin, without additional Ags or adjuvants, allowed development of an NOD mouse-specific, autoimmune encephalitis with variable primary-progressive, monophasic, and relapsing-remitting courses. T cells from diabetic donors transferred CNS disease to pertussis toxin-pretreated NOD.scid mice, with accumulation of CD3/IFN-gamma transcripts in the brain. Diabetes and MS appear more closely related than previously perceived. NOD mouse-specific, autoimmune encephalitis provides a new MS model to identify factors that determine alternative disease outcomes in hosts with similar autoreactive T cell repertoires.
PMID: 11160351
J Immunol 2001 Apr 1;166(7):4751-4756
T Cells of Multiple Sclerosis Patients Target a Common Environmental Peptide that Causes Encephalitis in Mice. Winer S, Astsaturov I, Cheung RK, Schrade K, Gunaratnam L, Wood DD, Moscarello MA, O'Connor PW, McKerlie C, Becker DJ, Dosch HM
The Hospital For Sick Children, Research Institute, Division of Neurology, St. Michael's
Hospital, and Division of Laboratory Animal Services, Sunnybrook Hospital, and Departments of Paediatrics and Medicine, University of Toronto Toronto, Ontario, Canada. Department of Pediatrics, Division of Endocrinology Children's Hospital of Pittsburgh University of Pittsburgh, Pittsburgh, PA 15260.
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, BSA(193), which was targeted by most MS but not diabetes patients. BSA(193) 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, BSA(193), in encephalitis-prone humans and rodents may imply a common endogenous ligand, targeted through antigenic mimicry.
PMID: 11254737
Letzte Änderung am 04.12.2011