Oxidative mitogenesis: Participation of CD2 antigen in the generation and/or transduction of obligatory accessory signals Academic Article Article uri icon

Overview

MeSH Major

  • Antineoplastic Combined Chemotherapy Protocols
  • Breast Neoplasms
  • Hemangioblasts
  • Hematopoietic Stem Cells
  • Vascular Endothelial Growth Factor Receptor-1
  • Vascular Endothelial Growth Factor Receptor-2

abstract

  • We investigated the role of cluster designation 2 (CD2) antigen in the activation of human T cells using either soluble phase or crosslinked monoclonal anti-CD2 antibodies, and oxidizing mitogens as probes. Soluble phase anti-CD2 inhibited oxidative mitogenesis when accessory signals were delivered with accessory cells and not when 12-O-tetradecanoylphorbol-13-acetate or interleukin 2 provided the required accessory signals. Soluble phase anti-CD2 also inhibited accessory cell-dependent increases in intracellular free calcium concentration and cell-to-cell contact among oxidizing mitogen-treated T cells and accessory cells. Crosslinked anti-CD2, on the other hand, generated the required accessory signals and functioned as an accessory cell substitute. Also, signals initiated by crosslinked anti-CD2 were able to replace accessory cell signals only, and not the mitogenic signals initiated with the oxidizing mitogens. Collectively, these findings indicate that the CD2 antigen participates in the generation and/or transduction of accessory signals obligatory for oxidative mitogenesis.

publication date

  • January 1988

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1016/0008-8749(88)90259-6

PubMed ID

  • 2897246

Additional Document Info

start page

  • 117

end page

  • 25

volume

  • 114

number

  • 1