Biomedical subjects

F Shirakawa

Publications and source records attributed to F Shirakawa.

42 records · Page 3Linked to original sources

PubMed1986

Requirement of macrophages (monocytes) for the induction of interleukin 2 receptors on B lymphocytes.

The role of macrophages (monocytes) for the induction of interleukin 2 receptors (IL 2R) on human B lymphocytes was studied by a direct immunofluorescence method with the use of a fluoresceinated anti-IL 2R monoclonal antibody and a flow cytofluorometer. Highly purified B lymphocytes alone did not induce IL 2R on their surface by stimulation with Staphylococcus aureus Cowan I, anti-mu antibody, or pokeweed mitogen. However, the addition of monocytes successfully induced IL 2R on B lymphocytes stimulated with these mitogens in a dose-dependent manner. Interleukin 1 (IL 1) produced by monocytes could partially replace the accessory function of monocytes. In accordance with these results, the proliferation of B lymphocytes and the differentiation to immunoglobulin-producing cells in response to IL 2 were also dependent on monocytes or IL 1. These results suggest that the accessory function of macrophages for IL 2-induced B cell activation is primarily on the induction of IL 2R on B lymphocytes.

B-Lymphocytes↗

PubMed1986

Calcium dependency in the growth of adult T-cell leukemia cells in vitro.

The effects of calcium, calcium antagonists, and calmodulin inhibitors on the growth of adult T-cell leukemia (ATL) cells were studied in vitro. Fresh ATL cells from patients and established ATL cell lines did not grow well in a low-calcium (less than 0.01 mM) medium. However, their growth was enhanced by the addition of calcium to the medium in a dose-dependent manner. The maximum response was induced at 4 mM calcium, which was higher than that of the normal serum calcium level, 2.5 mM. Other leukemia cells, except ATL, grew well in the low-calcium medium, and their growth was not enhanced by the addition of calcium. Calcium antagonists and calmodulin inhibitors inhibited the growth of ATL cells at the concentration of 10(-5)-10(-7) M, while they did not inhibit the growth of other leukemia cells. Furthermore, the expression of interleukin 2 receptors (Tac antigens) on ATL cells was also enhanced by calcium and was inhibited by calcium antagonists and calmodulin inhibitors. In accordance with these results, the increase of the extracellular calcium concentration resulted in the increase of the intracellular calcium concentration in ATL cells, but not in other leukemia cells. These results suggest that calcium and calmodulin play a critical role in regulating the growth of ATL cells.

Calcium↗

PubMed1986

Immunosuppressive factors from adult T-cell leukemia cells.

The mechanism of immunodeficiency in adult T-cell leukemia (ATL) patients was studied in vitro. Peripheral blood lymphocytes from ATL patients and ATL cell lines such as Hut 102, MT 1, and MT 2 were not activated to proliferate by the stimulation with concanavalin A and suppressed normal lymphocyte proliferative responses induced with concanavalin A when cultured together. The sera from ATL patients and the culture supernatants from ATL cells and ATL cell lines also suppressed normal lymphocyte proliferative responses induced with concanavalin A. By Sephacryl S-200 column chromatography, the suppressive factors were fractionated as a single peak with the molecular weights of 50,000 to 70,000. The suppressive factors were unstable to acid treatment but stable to the treatment with base, heat, freezing-thawing, and trypsin. The factors suppressed the production of interleukin 2 by T-cells and the responsiveness of T-cells to interleukin 2, but not the expression of interleukin 2 receptors on T-cells and the production of interleukin 1 by monocytes. These results suggest that the immunosuppressive factors produced by ATL cells have some roles in the induction of immunodeficient states in ATL patients.

Cell Line↗

PubMed1985

Reduced function of HLA-DR-positive monocytes in patients with systemic lupus erythematosus (SLE).

Accessory function of monocytes for T-cell activation was studied in patients with systemic lupus erythematosus (SLE). Nylon column-purified T cells alone were not activated to proliferate by stimulation with concanavalin A (Con A), but the addition of dish-adherent monocytes restored the T-cell response in a dose-dependent manner (accessory function). This accessory function is mediated by HLA-DR-positive monocytes. This accessory function of monocytes was markedly impaired in SLE patients. The dysfunction of monocytes was marked in an active stage of SLE but not in an inactive stage of SLE. Furthermore, SLE T cells were not fully activated with Con A in the presence of normal monocytes, suggesting that both monocyte and T-cell functions were impaired in SLE patients. The dysfunction of SLE monocytes was due to neither the development of suppressor monocytes nor the overproduction of prostaglandins, because SLE monocytes did not suppress the accessory function of normal monocytes and indomethacin did not restore the dysfunction of SLE monocytes. The percentage of HLA-DR-positive cells in a monocyte population was markedly decreased in active SLE patients and moderately decreased in inactive SLE patients. Thus, the impairment of accessory function of monocytes in SLE patients seems to be derived from a decrease in HLA-DR-positive monocytes. These results suggest that the dysfunction of HLA-DR-positive monocytes plays an important role in the pathogenesis of SLE.

Autoantibodies↗

PubMed1985

Decrease in HLA-DR-positive monocytes in patients with systemic lupus erythematosus (SLE).

Monocyte populations expressing HLA-DR antigens were studied in SLE patients by flow cytofluorometry with indirect immunofluorescence. Both the number of HLA-DR-positive monocytes and the expression of HLA-DR antigens on monocytes were markedly decreased in active SLE patients and were recovered to the normal level in inactive SLE patients. Because Ia-positive monocytes play a regulatory role for several immune responses, the decrease in HLA-DR-positive monocytes will result in abnormal regulations of immune responses and will play some critical role in the pathogenesis and the process of SLE.

Adult↗

PubMed1983

[Complication of therapeutic transcatheter hepatic artery embolization for hepatoma--case of developing an extensive acute gastric ulcer].

We report the development of an extensive acute gastric ulcer in a 60-year-old man following therapeutic transcatheter hepatic artery embolization for hepatoma. The unintentional occlusion of branches of the right gastric artery with refluxed Gelfoam fragments is thought to be responsible. This complication is probably rare, but should be kept in mind when therapeutic embolization of the hepatic artery is performed.

Acute Disease↗