We evaluated the hypothesis that serum IgE regulates neutrophil FcεRI expression in the same manner as described for other FcεRI + cells. FcεRI expression by neutrophils of 40 asthma subjects and 20 control subjects did not correlate with serum IgE levels, whereas FcεRI expression by basophils of the same subjects showed a highly significant correlation. The level of FcεRI expression by neutrophils of both asthma and control subjects was approximately 1% of that for basophil FcεRI expression. IgE + neutrophils were minimally detectable, and FcεRI α subunit was not detected in Western blots of neutrophil membranes and cytosol. The neutrophil FcεRI did not support antiIgE stimulated superoxide release or IgE-induced increase in neutrophil survival. We conclude that FcεRI expression by neutrophils of both asthma patients and control individuals is minimal at best and that, if present, neutrophil FcεRI expression, unlike that of other human FcεRI + cells, is not regulated by serum IgE.
We examined the ability of HIV‐1 infected PBMC to influence neutrophil function. Incubating neutrophils with supernatant of PHA‐activated PBMC that had been cultured with HIV‐1 for six days (HIV‐1+ culture supernatant) significantly increased neutrophil survival at 48 hr. Depletion of the HIV‐1 virions by centrifugation did not alter the pro‐survival activity of the HIV‐1+ culture supernatant. The HIV‐1+ culture supernatant also induced expression of HLA‐DR and CD64 by neutrophils. The induction of HLA‐DR paralleled induction of HLA‐DR expression by GM‐CSF. The HIV‐1+ culture supernatant, however, did not induce neutrophil expression of CD80, CD86, or CD40. The HIV‐1+ culture supernatant stimulated concentration‐dependent increases in neutrophil HLA‐DR and CD64 at supernatant concentrations containing 5 to 50 pg GM‐CSF/ml and 3 to 30 pg IFN‐γ/ml, respectively. Neutralizing anti‐GM‐CSF antibody inhibited HLA‐DR expression and neutralizing anti‐IFN‐γ antibody inhibited CD64 expression induced by the HIV‐1+ culture supernatant. These results indicate that HIV‐1‐infected PBMC can prolong neutrophil survival and potentially influence neutrophil immune activity through the production of GM‐CSF and IFN‐γ. Supported by NIH Grant R21 DE070170
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