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Blood, 15 August 2004, Vol. 104, No. 4, pp. 1083-1093.
Prepublished online as a Blood First Edition Paper on April 27, 2004; DOI 10.1182/blood-2003-08-2652.
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IMMUNOBIOLOGY
LFA-1 signaling through p44/42 is coupled to perforin degranulation in CD56+CD8+ natural killer cells
Omar D. Perez,
Dennis Mitchell,
Gina C. Jager, and
Garry P. Nolan
From the Baxter Laboratory for Genetic Pharmacology, Stanford University School of Medicine, Stanford, CA; and the Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA.
Leukocyte function antigen 1 (LFA-1) is essential for the formation of immune cell synapses and plays a role in the pathophysiology of various autoimmune diseases. We investigated the molecular details of LFA-1 activation during adhesion between cytotoxic cells and a target model leukemia cell. The cytolytic activity of a CD3–CD8+CD56+ natural killer (NK) subset was enhanced when LFA-1 was activated. In a comparison of LFA-1 ligands, intercellular adhesion molecule 2 (ICAM-2) and ICAM-3 promoted LFA-1–directed perforin release, whereas ICAM-1 had little effect. Ligand-induced LFA-1 clustering facilitated perforin release, demonstrating LFA-1 could regulate degranulation mechanisms. LFA-1 induced the activation of src family kinases, Vav1 and p44/42 mitogen-activated protein kinase (MAPK), in human CD56+ NK cells as evidenced by intracellular phospho-epitope measurements that correlated with effector-target cell binding and perforin-granzyme A–mediated cytolytic activity. These results identify novel, specific functional consequence of LFA-1–mediated cytolytic activity in perforin-containing human NK subsets.
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