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.

Acetyl LDL (modified low-density lipoprotein), which is thought to be taken up through scavenger receptor A (SR-A), rapidly induced the appearance of phosphotyrosine proteins in monocytic THP-l-derived macrophages in vitro. The two alternative forms of Lyn (pS3 and p56) were found to be tyrosine-phosphorylated within 30 s after the stimulation with acetyl LDL. The catalytic activity of Lyn measured by an in vitro kinase assay had also increased in acetyl LDL-stimulated THP-l-derived macrophages. Furthermore, Lyn could be coimmunoprecipitated with SR-A from the cell lysate. These observations suggest a functional and possible physical association of SR-A with Lyn in THP-l-derived maerophages, and also imply a possible involvement of Lyn in SR-A signal transduetion.

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Although reports of serious infections in clinical trials for rheumatoid arthritis (RA) with tocilizumab, anti-interleukin6 (IL-6) receptor antibody, have been relatively few, there is still some concern about infections. We report here two cases of patients who developed severe pneumonia during tocilizumab treatment for RA. Both patients initially presented with only minimal clinical symptoms and modest elevations in serum C-reactive protein. Tocilizumab might suppress the early inflammatory symptoms of pneumonia.

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