Akiteru Takeuchi

Human anticentriole autoantibody in patients with scleroderma and Raynaud's phenomenon.

Unique autoantibody was found in sera from two different patients that reacted with centrioles of both cultured mammalian cells and human peripheral leukocytes as detected by the indirect immunofluorescent method. Sera from the same individuals, one with scleroderma and the other suffering from Raynauds phenomenon, also stained the basal bodies of rat tracheal ciliated cells by the identical technique. Data from subsequent investigations have suggested that the antigen(s) involved in the reaction are water-insoluble protein(s) or polypeptide(s) associated with centrioles and are distinct from microtubular proteins or purine nucleoside phosphorylase.

[Efficacy of oxaprozin in the treatment of articular symptoms of Behçet's disease].

Behqets disease is an intractable disease with unknown causes which involves the mucosal membrane and skin of the eyes, the oral cavity and genital area. In Japan an estimated 10,000 patients suffer f rom this disease. Almost half of these patients are annoyed with articular symptoms. Occasionally, these articular symptoms may be protracted, making the treatment more difficult (1). The drug frequently used in treating these articular symtoms is colchicine. However, it is not free f rom problems in terms of safety. Moreover, most of the nonsteriodal antiinflammatory drugs introduced, heretofore, are rather ineffective. Oxaprozin (4,5-diphenyl-2-oxazolepropionic acid), a nonsteroidal antiinflammatory drug having a new structure, is now being developed by Taisho Pharmaceutical Co., Ltd., has recently drawn attention in Japan because of its long half life in human blood, potent analgesic and antiinflammatory actions and high degree of safety (2,3). In the present study the authors at tempted to evaluate the utility of oxaprozin in the treatment of articular symptoms associated with Behgets disease. The study subjects consisted of 5 patients (1 male and 4 females) with a complete type of Behgets disease. All of these patients

Inhibition of neutrophil chemotaxis by a monoclonal antibody (TM316).

A monoclonal antibody, TM316, IgM, was raised against the human monocytoid leukaemia cell line THP‐1, and was shown to inhibit polymorphonuclear leucocyte (PMN) chemotaxis. The molecular weight (MW) of the protein on the PMN membrane with which TM316 bound was about 78,000. TM316 inhibited the chemotactic response of human PMN induced by at least three kinds of chemotactic factors (activated serum, N‐formyl‐l‐methionyl‐l‐leucyl‐l‐phenylalanine (FMLP), and a lymphocyte‐derived chemotactic factor (LDCF)) to the same extent. The extent of inhibition of chemotaxis by TM316 was strongly correlated with the quantity of cellular surface antigen recognized by TM316, when a cell sorter was used for analysis. TM316 did not alter the number of Fc or complement receptors of PMN, nor did it affect luminol‐enhanced chemiluminescence(CL), lysosomal enzyme release, adherence, or superoxide anion generation by PMN. TM316 seemed to recognize a common surface antigen which was necessary only for the process of chemotaxis.

Inhibition of neutrophil and monocyte functions by the monoclonal antibody TM2

The ability of the monoclonal antibody termed TM2 to inhibit chemiluminescence generation by granulocytes and monocytes was examined. TM2 could inhibit the chemiluminescence generation of these cells when they were stimulated by all the stimuli presented. It seems that TM2 binds to the surface antigen of phagocytic cells which is important in the generation of free radicals.