We write to retract an interpretation in our Report,“Contribution of human α-defensin 1, 2, and 3 to the anti-HIV-1 activity of CD8 antiviral factor”(1), wherein we demonstrated that human α-defensin 1, 2, and 3 account for much of the anti-HIV-1 activity of the CD8 antiviral factor (CAF) that is not attributable to β-chemokines. Although the antiviral activity of human α-defensin has not been called into question, the cellular source of these α-defensins has been reinterpretated in light of more recent experiments. Our experiments were done using purified CD8 T cells from long-term nonprogressors or normal persons that were stimulated with anti-CD3 and anti-CD28 antibodies, recombinant interleukin-2, phytohemagglutinin, and irradiated allogeneic peripheral blood mononuclear cells (PBMC). This method of stimulating CD8 T cells had been commonly used by many groups working on CAF (2–7). However, in a follow-up attempt to define the specific subpopulation of CD8 T cells that produce α-defensins, we have found that in the absence of allogeneic irradiated PBMC (feeders), stimulated CD8 T cell supernatants do not contain α-defensins. Although it could be argued that an allogeneic stimulus is a prerequisite for α-defensin production by CD8 T cells, it is more likely that they are derived from a cell population residing within allogeneic feeders.

To pursue the exact source of α-defensins in allogeneic feeders, we positively selected individual cell populations from irradiated PBMC and subjected them to the aforementioned stimulation conditions in the absence of allogeneic exposure. α-Defensins were detected in the supernatants of CD4 and CD8 T cells and CD19 B cells. However, if the allogeneic PBMC feeders were first treated with an anti-CD15 monoclonal antibody to eliminate residual neutrophils before being subjected to irradiation, then α-defensins were no longer detectable in the supernatants of stimulated T or B cells. These findings suggest that under our experimental conditions, even minor degrees of neutrophil contamination could result in the detection of α-defensins in the culture supernatant of other cell populations.