Expression of neurotrophin receptors in normal and malignant B lymphocytes

Eur Cytokine Netw. 2000 Jun;11(2):283-91.

Abstract

In order to define a cellular model suitable for studying, in vitro, the molecular properties and functions of neurotrophin receptors in human lymphocytes, TrkA, TrkB, TrkC and p75(NTR) expression was investigated in a panel of EBV immortalized lymphoblastoid (LCL) and Burkitt lymphoma-derived cell lines (BLs) compared to primary B lymphocytes by RT-PCR and flow cytometric analysis. Our data show that trkA and trkB are transcribed in most B cell lines of normal and malignant origin. For several of them, we also gained first evidence of trkC expression in B cells. All cell lines and primary B cells lack p75(NTR) expression. These data suggest that neurotrophin receptors expression in the B cell lines correlates to some extent with the phenotypic maturation stage and endogenous viral activity levels. Our data suggest that TrkA and TrkB, once activated, provide a partial rescue from apoptosis, whereas TrkC stimulates the progression through the cell cycle without affecting cell survival. Finally, the identification of a number of cell lines showing single expression of one of the Trk receptors has disclosed the availability of a cellular tool for further studies on their function, and mechanisms of signal transduction in the B cell moiety in the absence of p75(NTR).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • B-Lymphocytes / metabolism*
  • Base Sequence
  • Burkitt Lymphoma / genetics
  • Burkitt Lymphoma / metabolism
  • Burkitt Lymphoma / pathology
  • Cell Line
  • DNA Primers / genetics
  • Gene Expression
  • Humans
  • In Vitro Techniques
  • Rats
  • Receptor, trkA / genetics
  • Receptor, trkB / genetics
  • Receptor, trkC / genetics
  • Receptors, Nerve Growth Factor / genetics*
  • Signal Transduction
  • Tumor Cells, Cultured

Substances

  • DNA Primers
  • Receptors, Nerve Growth Factor
  • Receptor, trkA
  • Receptor, trkB
  • Receptor, trkC