IL-18-induced CD83+CCR7+ NK helper cells

doi:10.1084/jem.20050128

Published 3 October 2005. doi:10.1084/jem.20050128
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 7, 941-953

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ARTICLE

IL-18–induced CD83⁺CCR7⁺ NK helper cells

Robbie B. Mailliard¹, Sean M. Alber², Hongmei Shen³^,7, Simon C. Watkins²^,4^,7, John M. Kirkwood⁵^,7, Ronald B. Herberman⁵^,7, and Pawel Kalinski¹^,4^,6^,7

¹ Department of Surgery, University of Pittsburgh
² Department of Cell Biology and Physiology, University of Pittsburgh
³ Department of Radiation Oncology, University of Pittsburgh
⁴ Department of Immunology, University of Pittsburgh
⁵ Department of Medicine, University of Pittsburgh
⁶ Department of Infectious Diseases and Microbiology, University of Pittsburgh
⁷ University of Pittsburgh Cancer Institute, Pittsburgh, PA 15213

CORRESPONDENCE Pawel Kalinski: kalinskip{at}upmc.edu

In addition to their cytotoxic activities, natural killer (NK)cells can have immunoregulatory functions. We describe a distinct"helper" differentiation pathway of human CD56⁺CD3^– NKcells into CD56⁺/CD83⁺/CCR7⁺/CD25⁺ cells that display high migratoryresponsiveness to lymph node (LN)–associated chemokines,high ability to produce interferon- ${gamma}$ upon exposure to dendriticcell (DC)- or T helper (Th) cell–related signals, andpronounced abilities to promote interleukin (IL)-12p70 productionin DCs and the development of Th1 responses. This helper pathwayof NK cell differentiation, which is not associated with anyenhancement of cytolytic activity, is induced by IL-18, butnot other NK cell–activating factors. It is blocked byprostaglandin (PG)E₂, a factor that induces a similar CD83⁺/CCR7⁺/CD25⁺LN-homing phenotype in maturing DCs. The current data demonstrateindependent regulation of the "helper" versus "effector" pathwaysof NK cell differentiation and novel mechanisms of immunoregulationby IL-18 and PGE₂.

Abbreviations used: Ag, antigen; PG, prostaglandin.

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