Common variable immunodeficiency associated with myelocathexis and altered membrane sodium-proton antiport

H. Gur*, R. Koldanov, A. Segal, G. Schiby, O. Spielberg, W. Koren

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Alterations in protein kinase C (PKC) activity have been implied in the pathogenesis of common variable immunodeficiency (CVID). We analyzed amiloride-sensitive red blood cell Na+/H+ exchange (sodium-proton antiport, SPA) and its response to protein kinase stimulation in a patient with CVID. Compared with healthy subjects or patients with sepsis, a unique pattern of SPA activation has been shown. The patient’s SPA was decreased and unresponsive to PKC stimulation, whereas stimulation by insulin, a tyrosine kinase activator, restored SPA activity. An alteration of serine-threonine phosphorylation is suggested as a possible mechanism for the immune failure.

Original languageEnglish
Pages (from-to)46-50
Number of pages5
JournalPathobiology
Volume65
Issue number1
DOIs
StatePublished - 1 Jan 1997
Externally publishedYes

Keywords

  • Immunodeficiency
  • Myelocathexis
  • Phosphorylation
  • Sodium-proton antiport

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