title: The significance of T cells, B cells, antibodies and macrophages against encephalomyocarditis (EMC)-D virus-induced diabetes in mice.
abstract: In order to clarify the significance of protective mechanisms against encephalomyocarditis (EMC) virus-induced diabetes in mice, we studied the relative importance of T cells, B cells, antibodies and macrophages in the prevention of virus-induced diabetes. Neither T cell-deficient athymic nude mice nor B cell-deficient microMT/microMT mice showed an enhanced clinical course of EMC-D virus-induced diabetes, indicating that neither T cells nor B cells played a major role in the protection against EMC-D-virus-induced diabetes. Transfer of a large amount of antiserum to EMC-D-virus-infected mice protected the development of diabetes only when transferred within 36 h of infection, the timing of which was earlier than that for the production of natural neutralizing antibodied. Since pretreatment of mice with the macrophage-activating immunopotentiator Corynebacterium parvum (CP) completely prevented the development of diabetes, we studied the clinical outcome of EMC-D-virus-infected mice pretreated with CP. Mice treated with CP showed reduced proliferation of EMC-D virus in the affected organs, including the pancreas, while the levels of development of neutralizing antibody and serum interferon were not enhanced compared with the controls. Finally, we studied the macrophages derived from mice pretreated with CP and found that they inhibited the growth of EMC-D virus in vitro more than those derived from non-treated and thioglycolate-treated mice. Taken together, it can be suggested that neither T cells nor B cells, which have to do with adaptive immunity, play a significant role in the pathogenesis of EMC-D-virus-induced diabetes, while innate immunity, which is dependent on activated macrophages, contributes to in vivo resistance against EMC-D-virus-induced diabetes.
authors.affiliation: Department of Medicine and Biosystemic Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
authors.forename: Etsushi
authors.initials: E
authors.lastname: Kounoue
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Izumi
authors.forename: Shuichiro
authors.initials: S
authors.lastname: Ogawa
authors.forename: Shiori
authors.initials: S
authors.lastname: Kondo
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Katsuta
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Akashi
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Niho
authors.forename: Mine
authors.initials: M
authors.lastname: Harada
authors.forename: Sadafumi
authors.initials: S
authors.lastname: Tamiya
authors.forename: Hironori
authors.initials: H
authors.lastname: Kurisaki
authors.forename: Seiho
authors.initials: S
authors.lastname: Nagafuchi
mesh_terms: D000818:Animals; D000914:Antibodies, Viral / Q000097:blood / Q000276:immunology* / Q000627:therapeutic use; D001786:Blood Glucose / Q000032:analysis; D018188:Cardiovirus Infections / Q000150:complications* / Q000276:immunology*; D003922:Diabetes Mellitus, Type 1 / Q000517:prevention & control*; D004686:Encephalomyocarditis virus / Q000276:immunology*; D007372:Interferons / Q000097:blood; D008214:Lymphocytes / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D008819:Mice, Nude; D009500:Neutralization Tests; D011425:Propionibacterium acnes / Q000276:immunology
chemical_list: D000914:Antibodies, Viral; D001786:Blood Glucose; D007372:Interferons