[The functional activity and count of the natural killer cells in patients with recently diagnosed diabetes mellitus types I and II]

Ter Arkh. 1989;61(10):104-6.
[Article in Russian]

Abstract

Eight patients with type I diabetes mellitus (D-I), seven patients with type II diabetes mellitus (D-11) and 8 healthy donors were examined. The disease standing did not exceed 1 year since the moment of the diagnosis establishment. The patients with D-I manifested activation of natural killers (NK) as compared to their activity in the donors and patients with D-II (76.05 +/- 6.5%, 52.33 +/- 9.55% and 55.39 +/- 10.63%, respectively, p less than 0.01) in the presence of the attenuated response of NK to interleukin-2 and alpha-interferon, determined by NK prestimulation. The amount of NK (CD16-positive) in D-I was significantly less than in the donors and patients with D-II. The high activity of NK in D-I correlated with an increase of receptor expression for transferrin on the mononuclear cells of peripheral blood. At the same time 5 out of the 8 patients with D-I and 2 patients with D-II out of the 7 demonstrated the rise of serum alpha-interferon (in the titer 1:40 and over). Activation of NK and the rise of serum interferon may be due to viral etiology of the disease and may play a role in the autoimmune process in patients suffering from D-I.

Publication types

  • Comparative Study
  • English Abstract

MeSH terms

  • Adolescent
  • Adult
  • Cytotoxicity Tests, Immunologic / methods
  • Diabetes Mellitus, Type 1 / etiology
  • Diabetes Mellitus, Type 1 / immunology*
  • Diabetes Mellitus, Type 2 / etiology
  • Diabetes Mellitus, Type 2 / immunology*
  • Female
  • Humans
  • Interferon Type I / pharmacology
  • Interleukin-2 / pharmacology
  • Killer Cells, Natural / drug effects
  • Killer Cells, Natural / immunology*
  • Leukocyte Count
  • Male
  • Middle Aged
  • Recombinant Proteins / pharmacology
  • T-Lymphocytes, Cytotoxic / drug effects
  • T-Lymphocytes, Cytotoxic / immunology

Substances

  • Interferon Type I
  • Interleukin-2
  • Recombinant Proteins