Activated phenotype seen in reduced, specific natural killer cells in active granulomatosis with polyangiitis

Recently published results showed an activated and altered phenotype, as well as deficient overall natural cytotoxicity, among patients who have active granulomatosis with polyangiitis with reduced numbers of CD56^dim natural killer cells.

Wolfgang Merkt, MD, in the division of rheumatology at Universität Heidelberg, and colleagues analyzed two peripheral blood lymphocyte subsets from two patient cohorts diagnosed with granulomatosis with polyangiitis (GPA) and grouped according to activity state. Researchers performed a separate analysis and a combined analysis of natural killer cell counts and percentages.

Wolfgang Merkt

Despite normal percentages due to lymphopenia, results showed a lower count of natural killer cells than the lower limit of normal in active GPA in the second cohort. Researchers found natural killer cells counts were significantly higher in remission. However, researchers did not find this in other lymphocyte counts. In a combined analysis of both cohorts, results showed natural killer cell counts decreased in active GPA but increased percentages in long-term remission. A follow-up measurement of six patients showed natural killer cell percentages increased during successful induction therapy, according to results.

Through a multicolor analysis in the second cohort, researchers found the CD56^dim subset in active GPA decreased natural killer cell counts, downregulated the Fc-receptor CD16, and upregulated the adhesion molecule CD54, the chemokine receptor CCR5 and the activating receptor NKG2C, which were unaltered or marginally altered in remission. Results showed no change in all other receptors investigated. Although researchers could not detect natural cytotoxicity in most patients with active GPA, it was restored in remission. – by Casey Tingle

Disclosures: Merkt received an honorarium from Roche. Please see the full study for a list of all other authors’ relevant financial disclosures.

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Source:

Merkt W, et al. Arthritis Res Ther. 2016;doi:10.1186/s13075-016-1098-7.