Kati
Patient in training
- Messages
- 5,497
Assessment of the Fc receptor CD16A of NK cells of CFS patients for potential to mediate ADCC activity (HUM1P.303)
http://www.jimmunol.org/content/194/1_Supplement/52.28.short
Abstract:
Natural killer (NK) cytotoxicity of chronic fatigue syndrome (CFS) patients is decreased, as reported by several laboratories.
This observation led us to query whether the NK cells also lack antibody-dependent cell-mediated cytotoxicity (ADCC).
NK cells have the IgG Fc-receptor CD16A that mediates ADCC.
To assess potential ADCC effectors, we examined the peripheral blood of 11 CFS patients from a Lake Tahoe cohort that met the Fukuda standards for CFS and had low SF36 scores.
Healthy controls were age- and gender-matched. We stained peripheral blood cells for CD16A with mAb clone 3G8 and for CD3, CD56, and perforin, then assessed the cells by flow cytometry.
We found that the percentages of NK cells expressing CD16A were slightly lower for CFS patients 86.0+/-11.5% vs. controls 93.0+/-6.6% (P=0.08).
The median fluorescent indices (MFIs) of CD16A were lower,72% of the values for the CFS patients, 9342+/-3233 vs. control 12929+/-4425, though not statistically significant (P<0.17). Intracellular staining for perforin in the CD16Apos cells was similar for patients and controls.
Our data indicate that a larger sampling of CFS patients vs. controls is required to determine if the fractions of CD16Apos NK cells and the levels of CD16A on these cells differs.
These two observations are both in the direction of compromising ADCC activity of patients.
In addition, a bias in F over V allelic variants of CD16A might add to impairment, since the F allele confers reduced ADCC.
http://www.jimmunol.org/content/194/1_Supplement/52.28.short
Abstract:
Natural killer (NK) cytotoxicity of chronic fatigue syndrome (CFS) patients is decreased, as reported by several laboratories.
This observation led us to query whether the NK cells also lack antibody-dependent cell-mediated cytotoxicity (ADCC).
NK cells have the IgG Fc-receptor CD16A that mediates ADCC.
To assess potential ADCC effectors, we examined the peripheral blood of 11 CFS patients from a Lake Tahoe cohort that met the Fukuda standards for CFS and had low SF36 scores.
Healthy controls were age- and gender-matched. We stained peripheral blood cells for CD16A with mAb clone 3G8 and for CD3, CD56, and perforin, then assessed the cells by flow cytometry.
We found that the percentages of NK cells expressing CD16A were slightly lower for CFS patients 86.0+/-11.5% vs. controls 93.0+/-6.6% (P=0.08).
The median fluorescent indices (MFIs) of CD16A were lower,72% of the values for the CFS patients, 9342+/-3233 vs. control 12929+/-4425, though not statistically significant (P<0.17). Intracellular staining for perforin in the CD16Apos cells was similar for patients and controls.
Our data indicate that a larger sampling of CFS patients vs. controls is required to determine if the fractions of CD16Apos NK cells and the levels of CD16A on these cells differs.
These two observations are both in the direction of compromising ADCC activity of patients.
In addition, a bias in F over V allelic variants of CD16A might add to impairment, since the F allele confers reduced ADCC.