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Helicobacter pylori infection might prove the hygiene hypothesis in multiple sclerosis
  1. Jun-ichi Kira
  1. Correspondence to Dr Jun-ichi Kira, Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; kira{at}neuro.med.kyushu-u.ac.jp

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In many developed countries, the incidence of autoimmune diseases and allergic/atopic disorders are rapidly increasing. The former is regarded as a T helper (Th)1/Th17 disease while the latter is considered a Th2 disease. It is curious that the incidence of Th1/Th17 and Th2 diseases have increased simultaneously, given that Th1/Th17 cells and Th2 cells counteract each other. This inconsistency is explained by the ‘hygiene hypothesis’.1 Frequent infections in poor sanitary conditions may facilitate the development of the immune effector and immune regulatory systems. Overactivation of effector lymphocytes, macrophages and neutrophils during infection should be removed rapidly once infectious pathogens are eradicated; otherwise, these immune cells can cause bystander destruction of the neighbouring uninfected tissues. As a result, repeated infection might shape immune regulatory systems. The underdevelopment of immune regulatory systems because of infrequent infections during early life might prevent activated Th1/Th17 cells and Th2 cells from being controlled, resulting in the increased frequency of autoimmune diseases and allergic/atopic diseases later in life.1

Multiple sclerosis (MS) is assumed to be an autoimmune disease targeting central nervous system (CNS) myelin, whose pathogenesis is thought to involve a complex interplay …

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