Leptin inhibits stress-induced apoptosis of T lymphocytes

Clin Exp Immunol. 2002 Apr;128(1):21-6. doi: 10.1046/j.1365-2249.2002.01797.x.

Abstract

Leptin, which is secreted by adipocytes, the placenta and the stomach, not only controls appetite through leptin receptors in the hypothalamus but also regulates cell-mediated immunity. In this study we have demonstrated that continuous injection of leptin prevents the reduction in lymphocyte numbers normally observed in fasted and steroid-injected mice. Consistent with leptin-induced protection, we observed up-regulation of the bcl-xL gene as a result of signal transduction via leptin receptors on lymphocytes. We suggest that leptin might contribute to the recovery of immune suppression in malnourished mice by inhibiting lymphocyte apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Carrier Proteins / biosynthesis
  • Carrier Proteins / genetics
  • Cell Nucleus / ultrastructure
  • DNA Fragmentation
  • Fasting
  • Female
  • Hybridomas
  • Hydrocortisone / antagonists & inhibitors
  • Immunocompromised Host
  • Leptin / genetics
  • Leptin / pharmacology*
  • Lymphocyte Count
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • RNA, Messenger / biosynthesis
  • Receptors, Cell Surface*
  • Receptors, Leptin
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / ultrastructure
  • bcl-X Protein

Substances

  • Bcl2l1 protein, mouse
  • Carrier Proteins
  • Leptin
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger
  • Receptors, Cell Surface
  • Receptors, Leptin
  • bcl-X Protein
  • leptin receptor, mouse
  • Hydrocortisone