TLR signaling and effector functions are intact in XLA neutrophils

Thomas U. Marron, Kaileen Rohr, Monica Martinez-Gallo, Joyce Yu, Charlotte Cunningham-Rundles*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

22 Citations (Scopus)

Abstract

Toll-like receptors (TLRs) are essential components of the innate immune system, and their ligands are important activators of neutrophils. Bruton's tyrosine kinase (Btk) has been reported to mediate signaling through toll-like receptors (TLRs) in many cell types, however, the role of Btk in TLR activation of neutrophils remains unclear. Impaired TLR-induced neutrophil function was found in mice with loss of Btk and in humans with TLR-signaling defects, but the integrity of TLR pathways in X-linked agammaglobulinemia (XLA) neutrophils has not been assessed. In this study LPS (TLR4) or an imidazoquinoline compound (TLR7/8) activated XLA neutrophil shedding of surface CD62L, and phosphorylated MAP kinases p38, JNK and ERK. TLR activation also induced normal respiratory burst and retarded apoptosis for XLA neutrophils, comparable to normal controls. These data demonstrate that the loss of Btk in XLA neutrophils does not impair functional responses to TLR signals.

Original languageEnglish
Pages (from-to)74-80
Number of pages7
JournalClinical Immunology
Volume137
Issue number1
DOIs
Publication statusPublished - Oct 2010

Keywords

  • Bruton's tyrosine kinase
  • BTK
  • Neutrophils
  • Respiratory burst
  • TLR
  • Toll-like receptors
  • X-linked agammaglobulinemia
  • XLA

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