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Biomedical subjects

F Stiekema

Publications and source records attributed to F Stiekema.

3 recordsLinked to original sources

The crucial role of human dendritic antigen-presenting cell subsets in nickel-specific T-cell proliferation.

In the majority of patients, allergic nickel contact dermatitis is associated with a proliferative response of peripheral blood T lymphocytes to nickel sulfate. Optimal proliferation was found in a concentration range of 1-2 X 10(-4) M nickel sulfate. Nickel-specific response of purified peripheral blood T cells requires the presence of antigen-presenting cells (APC). Both peripheral blood monocytes and skin-derived epidermal cells could function as APC, but epidermal cells were shown to be more potent than monocytes. By testing FcR+ monocytes and FcR- circulating dendritic cells for their antigen-presenting capacities, it was found that the critical APC within the fraction of monocytes is the circulating dendritic cell. Testing highly purified T6+ (CD 1) skin-specific dendritic cells (Langerhans cells, LC) and T6- epidermal cells as APC, the critical APC within the fraction of epidermal cells appeared to be the LC. The crucial role of LC was stressed in experiments using T cells from patients exhibiting a positive patch test to nickel but a low or absent proliferative response to nickel by unpurified peripheral blood cells. Whereas addition of peripheral blood APC was ineffective, addition of LC to purified peripheral T cells was shown to overcome this low responsiveness to nickel. These results indicate the crucial role of dendritic APC subsets in nickel-specific T-cell proliferation.

Antigen-Presenting Cells

Differential requirements for rabbit dendritic cells and macrophages in T lymphocyte proliferation induced by various mitogens.

Dendritic cells have been isolated from rabbit lymph nodes. Morphologically and phenotypically, they resemble dendritic cells from the mouse and rat. A comparison was made of the accessory cell function of dendritic cells and peritoneal macrophages in T-cell proliferation induced by phytohaemagglutinin (PHA) or Con A, or by a simultaneous treatment with the enzymes neuraminidase and galactose oxidase (NaGo). Dendritic cells seemed to be more effective than macrophages as accessory cells in these assays. However, macrophages suppress lymphocyte proliferation through the release of oxidating agents and production of prostaglandins. Elimination of this suppressive effect of the macrophages by addition of a combination of 2-mercaptoethanol (2-ME) and indomethacin in PHA-induced cell proliferation resulted in a much higher support by macrophages, giving results that were comparable to those obtained with dendritic cells, but in NaGo-induced proliferation, macrophages were still not as effective as dendritic cells in the presence of the drugs. Experiments in diffusion culture vessels and with interleukin-1-containing macrophage supernatants showed that support by accessory cells can be mediated by soluble factors in PHA-induced proliferation. In contrast, in NaGo-induced proliferation, lymphocytes and accessory cells have to interact directly.

Animals