Interleukin‐6 (IL‐6) was found to be a growth factor of renal cell carcinomas. Furthermore, renal cell carcinomas freshly isolated from the patients expressed mRNA of IL‐6 and secreted biologically active IL‐6 under the culture conditions where the tumor cells could grow, but they did not produce IL‐6 nor proliferate in the absence of fetal calf serum. The production of IL‐6 by the tumor cells was also demonstrated by immunostaining of the IL‐6‐producing cells utilizing anti‐IL‐6 antiserum. Moreover, anti‐IL‐6 antiserum specifically inhibited the in vitro tumor growth. All data indicated that IL‐6 functions as an in vitro autocrine growth factor of renal cell carcinomas.

In order to clarify the regulatory mechanisms of periodontal regeneration by basic fibroblast growth factor (bFGF), effects of bFGF on proliferation, alkaline phosphatase activity, calcified nodule formation and extracellular matrix synthesis of human periodontal ligament (PDL) cells were examined in this study. bFGF enhanced the proliferative responses of PDL cells in a dose-dependent manner. The maximum mitogenic effect of bFGF on PDL cells was observed at the concentration of 10 ng/ml. In contrast, bFGF inhibited the induction of alkaline phosphatase activity and the mineralized nodule formation by PDL cells. Moreover, employing the reverse transcription-polymerase chain reaction (RT-PCR) technique, we observed that the levels of laminin mRNA of human PDL cells was specifically upregulated by bFGF stimulation, but that of type I collagen mRNA was downregulated. On the other hand, the expression of type III collagen and fibronectin mRNA were not altered even when the cells were activated by bFGF. These results suggest that suppressing cytodifferentiation of PDL cells into mineralized tissue forming cells, bFGF may play a role in wound healing by inducing growth of immature PDL cells and that in turn accelerates periodontal regeneration.

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Immunoglobulin (Ig) G subclasses in anti-basement membrane zone (BMZ) autoantibodies found in the sera of bullous pemphigoid (BP) and in anti-intercellular substance (ICS) autoantibodies of pemphigus were investigated using immunofluorescent (IF) staining. In BP, IgG4, IgG1, and IgG2 were detected in 13, 5 and 6 of 15 patients, respectively; IgG3 was not detected. In pemphigus, IgG4 was detected in all of 10 patients, IgG1 in 7, IgG2 in one, and IgG3 in one patient, respectively. In both BP and pemphigus, the most prominent subclass in intensity of IF staining was IgG4. Although one BP and one PV patient had only IgG4 autoantibodies, C3 deposition was detected. The quantification of IgG subclasses in the sera of the patients was performed by enzyme-linked immunosorbent assays (ELISA). Serum levels of IgG4 in both BP and pemphigus were elevated approximately 3-fold over those in normal controls; those of whole IgG and IgG1-3 were not significantly elevated. Using direct IF staining, the deposition of C3 at the BMZ and at the ICS was demonstrated in 9 of 10 BP and in 3 of 8 pemphigus patients, respectively. The prominent IgG subclasses of anti-BMZ and anti-ICS antibody were IgG4, a noncomplement-fixing antibody, suggesting that the deposition of C3 in the lesional skin occurred via the alternative pathway, or that small amounts of IgG1-3 subclass autoantibodies activated the classical pathway.