Objective. CD14؉,CD16؉ monocytes, identified as a minor population of monocytes in human peripheral blood (PB), have been implicated in several inflammatory diseases. We undertook this study to investigate the relevance of this phenotype to joint inflammation in rheumatoid arthritis (RA).Methods Results. The mean ؎ SD frequency of CD14؉,CD16؉ blood monocytes was significantly increased in RA patients (11.7 ؎ 5.6%; n ‫؍‬ 105) compared with healthy controls (9.5 ؎ 2.2%; n ‫؍‬ 15) (P < 0.01), and the patient group with an increased frequency of CD16؉ monocytes (>13.9%) had active disease, as defined by increased counts of tender and swollen joints, levels of acute-phase reactants, and titers of rheumatoid factor. The response to drug therapy correlated with changes in the frequency of this phenotype. The expression of CD16 on SF monocytes from RA patients was markedly elevated compared with the expression on PB monocytes. CD16 expression on RA blood monocytes was augmented in vitro by IL-10, M-CSF, and TGF␤1. Plasma concentrations of these cytokines and of sCD14 were significantly higher in RA patients with high CD16؉ monocyte frequencies than in those with low CD16؉ monocyte frequencies or in healthy controls. CD14؉,CD16؉ monocytes expressed higher levels of CCR1, CCR5, and ICAM-1 than did regular CD14؉؉,CD16؊ monocytes, particularly in active RA.Conclusion. These results indicate that the maturation of blood monocytes into tissue-infiltrative CD16؉ cells before entry into the joint, induced by cytokine spillover from the inflamed joint, may contribute to the persistent joint inflammation of RA.In human peripheral blood (PB), two monocyte subpopulations with distinct functional properties have been defined by their expression of CD14 and CD16 molecules (1,2). CD14 is the receptor for complexes of lipopolysaccharide (LPS) and LPS-binding protein (3). CD16 is the low-affinity receptor for the Fc region of IgG (Fc␥ receptor type III [Fc␥RIII]) and plays an important role in the clearance of immune complexes (4). Significant expression of CD16 was originally found to be induced on blood monocytes during their differentiation to macrophages in culture, while expression of other Fc␥R decreased (5), but 2-color immunofluorescence analysis with antibodies against CD14 and CD16 has revealed the existence of CD16-expressing monocytes with weak CD14 staining in PB. These CD14ϩ,CD16ϩ cells show typical monocyte morphology with irregular nuclei and account for ϳ10% of circulating monocytes in healthy individuals (1,2,6).

The functionality of immune cells is manipulated within the ocular microenvironment to protect the sensitive and non-regenerating light-gathering tissue from the collateral damage of inflammation. This is mediated partly by the constitutive presence of immunomodulating neuropeptides. Treating primary resting macrophages with soluble factors produced by the posterior eye induced co-expression of Arginase1 and NOS2. The neuropeptides alpha-melanocyte stimulating hormone and Neuropeptide Y alternatively activated the macrophages to co-express Arginase1 and NOS2 like myeloid suppressor cells. Similar co-expressing cells were found within healthy, but not in wounded retinas. Therefore, the healthy retina regulates macrophage functionality to the benefit of ocular immune privilege.

Background/Aims: Circulating CD14+CD16+ monocytes, a potent phagocytosing and antigen-presenting monocyte population, have been reported to be expanded in patients on hemodialysis (HD). In this study, changes in the population of CD14+CD16+ monocytes were analyzed during a single session of HD therapy, and the influence of dialyzer membrane materials on these monocytes was investigated. Methods: Nine patients were hemodialyzed using regenerated cellulose (RC) membranes and thereafter polysulfone (PS) membranes. Peripheral blood cells were taken from these subjects, and these cells were stained with anti-CD14 and anti-CD16 antibodies. The percentages of CD14- and CD16-expressing monocytes were analyzed by two-color flow cytometric analysis. Moreover, the serum soluble CD14 (sCD14) levels were measured with an ELISA kit. Results: It was found that CD14+CD16+ monocytes before HD were significantly increased in patients on HD as compared to healthy controls. In the RC group, CD14+CD16+ monocytes were decreased at both 30 and 240 min after the initiation of HD. The reduction rate of CD14+CD16+ monocytes in the RC group was higher than that in the PS group. There was no significant difference in sCD14 levels between the two groups. Conclusion: Monocytes are activated in patients on HD. Furthermore, the population of CD14+CD16+ monocytes was stimulated to a greater extent during HD in the RC group than in the PS group. The significant reduction in CD14+CD16+ monocytes by RC membranes indicated that the level of CD14+CD16+ monocytes is a sensitive marker for the biocompatibility of HD membranes.

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