Employing nylon wool-adherent cells as antigen-presenting cells(APC), it was demonstrated that T-lymphocyte could respond sufficiently well to PPD-pulsed APC sharing at least one of the HLA-DR antigens of the T-lymphocyte donor.
Antisera against HLA-DR but not HLA-A and -B antigens were shown to be able to block this proliferative responses when PPD-pulsed APC had been pretreated with anti-HLA-DR antisera.
These results indicate that HLA-DR antigens paly a functional role in the antigen-present-ation.

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A marked decrease of T lymphocytes and Tγ was demonstrated in 8 patients with IBL. Null lymphocytes increased makedly in IBL. Null lymphocytes were present in the Fr I fractionated by gumi accaci density gradient centrifugation of blood lymphocytes. The PHA blastoid transformation of IBL blood lymphocytes slightly decreased. A marked decrease of Ts was demonstrated in blood and lymphnode lymphocytes in IBL. The development of cIg⁺ cells by PWM stimulation from IBL lymphnode B lymphocytes was demonstrated, but it was resistant to the regulation of normal Ts. No lymphocytotoxin was demonstrated in IBL serum. The induction of Ts activity by the ConA activation of IBL lymphocytes was markedly decreased. Null lymphocytes of Fr I showed the helper effect to the development of clg⁺ cells from normal B lymphocytes by the PWM stimulation.

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Immunological studies were carried out on ten patients with the aplastic anemia with hyperplasia of erythroblasts (AAHE). A decrease of E-RFC and Thy⁺ cells and an increase of Fc (γ) receptor positive (FcR⁺) cells, Tγ, Tpμ and null lymphocytes were demonstrated in blood lymphocytes of patients with AAHE. Tγ, FcR⁺ cells and K cells were increased in the bone marrow lymphocytes subpopulation in patients with AAHE. The antibody dependent cell-mediated cytotoxity to patelets, erythroblasts and immature granulocytes was positive in patients with AAHE. Bone marrow lymphocytes from patients with AAHE produced IgG in vitro by the stimulation of platelet membrane antigens, erythroblast membrane antigens and immature granulocyte membrane antigens. A decrease of suppressor T cells (Ts) was present in blood lymphocytes of patients with AAHE. The in vitro development to Ig producing cells of bone marrow lymphocytes by PWM stimulations was increased in AAHE. The sensitivity of bone marrow lymphocytes to normal Ts was decreased in AAHE. These results indicate that AAHE is the autoimmune diseases which might be cause probably by the similar mechanism with that in Hashimoto's thyroidits. AAHE should be termed as the autoimmune pancytopenia.

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Mitogen induced cell-mediated cytotoxicity (MICC) of human peripheral blood granulocytes (PMN) and lymphocytes (PBL) were studied by employing chicken erythrocytes as targets. MICC mediated by both effectors revealed similar dose-response and temperature-dependency was only significantly induced by T cell mitogen but not by B cell mitogen. PMN were found to exhibit more effective cytotoxicity than PBL in our study. The direct contact of effectors and targets was essential to induce MICC. Participation of erythrophagocytosis was not supported in MICC activity and supernatant obtained from cultivated effector-target-lectin ligand or soluble sonicated PMN lysate did not affect MICC. Additionally, MICC inhibition study was performed in an attempt to disclose certain possible effector mechanisms of MICC. The results indicated that membrane active agents, anti-tubulin, anti-microfilament, EDTA, local anesthetics and soluble immune complex considerably suppressed the MICC activity. DNA-inhibitor and specific sugar had moderate effect whereas gold salt, insoluble immune complex or membrane Na⁺-K⁺-ATPase inhibitor showed little effect on the activity. These observations provided us to conclude that the full expression of MICC required functionally preserved lectin reactive membrane receptors, intact cytoskeletal system, active DNA synthesis and presence of divalent cations.

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Polymyalgia rheumatica (PMR) was a rare rheumatic disease in Japan, nevertherless common in European and American caucasians. In Japan recently PMR is one of well established rheumatic diseases. We experienced four cases of PMR in our rheumatic clinic for the past five years. Only one of them was male and the youngest case was 41 years of age. Most of them presented with myalgic pains of proximal areas of trunks, continuous fever and emaciation. It took for long time (3 months to 4 years) inorder to diagnose PMR. The previous diagnosis were fever of unknown origin (FUO) or some collagen diseases. One of them was a case associated with temporal arteritis, which was diagnosed from a biopsy finding of temporal artery. Other case was strongly suspected to be associated with temporal arteritis. All of them well responded to corticosteroid administration, and myalgic pain and fever episodes disappered promptly. It was difficult to taper off the corticosteroid in all cases. In serological examination it was showed that one of them had the antibody against DNA.

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