Interferon-inducible protein-10 and lymphotactin induce the chemotaxis and mobilization of intracellular calcium in natural killer cells through pertussis toxin-sensitive and -insensitive heterotrimeric G-proteins

FASEB J. 1997 Aug;11(10):765-74. doi: 10.1096/fasebj.11.10.9271361.

Abstract

We show here that interferon-inducible protein-10 (IP-10), an ELR lacking CXC chemokine, and the C chemokine lymphotactin (Ltn) induce the chemotaxis and calcium mobilization in IL2-activated NK (IANK) and CC chemokine-activated NK (CHAK) cells. Cross-desensitization experiments show that IP-10 or Ltn use receptors not shared by other C, CC, or CXC chemokines. The chemotaxis induced by either IP-10 or Ltn for both cell types is inhibited upon pretreatment of these cells with pertussis toxin (PT). Also, Ltn-induced [Ca2+]i in IANK but not in CHAK cells is inhibited upon pretreatment with PT, whereas IP-10-induced [Ca2+]i in IANK and CHAK cells is inhibited upon pretreatment with this toxin. These results suggest important roles for PT-sensitive and -insensitive G-proteins in IP-10-induced and Ltn-induced chemotaxis and calcium fluxes in activated NK cells. This was further implicated after streptolysin O permeabilization of CHAK and IANK cells and after introduction of inhibitory antibodies to the PT-sensitive Gi and Go or the PT-insensitive Gq. Our results suggest that IP-10 and Ltn receptors are coupled to Gi, Go, and Gq in IANK cells and to Gi and Gq in CHAK cells, with a possible low coupling of IP-10, but not of Ltn, receptors to Go in these cells. Together, these results show that IP-10 and Ltn-dependent chemotaxis and calcium mobilization may differentiate at the level of receptor coupling to the heterotrimeric G-proteins.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Calcium / physiology
  • Cells, Cultured
  • Chemokine CCL5 / physiology
  • Chemokine CXCL10
  • Chemokines / physiology*
  • Chemokines, C*
  • Chemokines, CXC*
  • Chemotaxis, Leukocyte*
  • Cytoplasm / metabolism
  • GTP-Binding Proteins / physiology*
  • Humans
  • Immunologic Techniques
  • Killer Cells, Natural / physiology*
  • Lymphocyte Activation
  • Lymphokines / pharmacology*
  • Pertussis Toxin*
  • Receptors, Cell Surface / physiology
  • Receptors, Immunologic / physiology
  • Second Messenger Systems
  • Sialoglycoproteins / pharmacology*
  • Signal Transduction
  • Virulence Factors, Bordetella / pharmacology*

Substances

  • Chemokine CCL5
  • Chemokine CXCL10
  • Chemokines
  • Chemokines, C
  • Chemokines, CXC
  • Lymphokines
  • Receptors, Cell Surface
  • Receptors, Immunologic
  • Sialoglycoproteins
  • Virulence Factors, Bordetella
  • XCL1 protein, human
  • lymphotactin
  • Pertussis Toxin
  • GTP-Binding Proteins
  • Calcium