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Anti-asialo GM1 antibody suppression of cyclophosphamide-induced diabetes in NOD mice.

Authors
  • Maruyama, T
  • Watanabe, K
  • Takei, I
  • Kasuga, A
  • Shimada, A
  • Yanagawa, T
  • Kasatani, T
  • Suzuki, Y
  • Kataoka, K
Type
Published Article
Journal
Diabetes research (Edinburgh, Scotland)
Publication Date
May 01, 1991
Volume
17
Issue
1
Pages
37–41
Identifiers
PMID: 1823558
Source
Medline
License
Unknown

Abstract

To elucidate the role of natural killer (NK) cells in the pathogenesis of diabetes in the non-obese diabetic (NOD) mouse, we examined whether or not cyclophosphamide-induced diabetes occurs in NOD mice intraperitoneally (i.p.) injected with anti-asialo GM1 antibody. Two weeks after a single intraperitoneal injection of cyclophosphamide, none of the 24 NOD mice which had previously been treated with antiasialo GM1 antibody, 2-3 times per week for either 2 or 3 weeks, had developed indications of diabetes such as glycosuria or a high plasma glucose level. On the other hand, signs of diabetes were found in 10 of 24 control NOD mice injected with normal rabbit Ig instead of anti-asialo GM1 antibody (p less than 0.01). The NK cell activities of spleen cells from anti-asialo GM1 antibody-treated mice were significantly lower than those of control mice (p less than 0.01). Flowcytometry analysis demonstrated that anti-asialo GM1 antibody-positive cells had disappeared from the spleens of anti-asialo GM1 antibody-injected mice but no suppression of CD8+ and CD4+ cells could be demonstrated. These observations suggest that NK cells are involved in the development of diabetes in NOD mice.

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