Serum levels of immunosuppressive acidic protein (IAP) of various diseases were measured by single radial immunodiffusion method. 2 to 10 times higher levels than normal values (394μg/ml) were found in patients with various cancers, SLE, scleroderma, cryptogenic pulmonary fibrosis, chronic bronchitis, pulmonary tuberculosis, pneumonia and bronchial asthma at these exacerbation or active stages. There were good correlations between IAP levels and blood sedimentation rate, α₂-globulin values (p<0.001). The higher IAP levels of patients with cancer than 2, 000μg/ml were reflected the decreased ability of hypersensitivity to PPD or DNCB and poorer prognosis. It is suggested that serum IAP levels could be one of good indicators for evaluating the immunological activities of patients with various diseases.

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Lymphocytotoxic antibodies were detected by ⁵¹Cr release assay. This method showed the specificity and sensitivity compatible with Terasaki's microcytotoxicity test. Coefficient of variation in this method was reproducibly less than 15%. ⁵¹Cr release assay was thus a simple and useful method for the detection of lymphocytotoxic antibodies. Using this method, the antibodies were demonstrated in sera of 87% of patients with SLE, 67% with Sjögren's syndrome, 61% with rheumatoid arthritis, 59% with progressive systemic sclerosis, 30% with polymyositis and dermatomyositis and 49% with myasthenia gravis.

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Lymphocytotoxic antibodies are demonstrated with high incidence in the sera of patients with autoimmune diseases including systemic lupus erythematosus, rheumatoid arthritis and myasthenia gravis.
The present report describes biologic characteristics of the antibodies found in these autoimmune diseases. Lymphocytotoxic antibodies were first proved to be specific for T lymphocytes and their specificity against human T cell subsets was thus investigated. IgG-Fc receptor bearing cells (T_γ cells) were separated from T_γ-depleted cells (T_non-γ cells) according to the former capacity to form rosettes with ox red blood cells sensitized by IgG antibodies. Lymphocytotoxic antibodies obtained from the sera of patients with SLE killed mostly T_γ cells, while those from rheumatoid arthritis and myasthenia gravis showed a preferential reactivity against T_non-γ cells.
After in vitro allosensitization, specific allogeneic cell-mediated lympholysis mediated by human peripheral blood lymphocytes. When normal T lymphocytes were pretreated with complement and the sera containing lymphocytotoxic antibodies before mixed lymphocyte reaction, the killer cell activity was augumented in cases with SLE and rheumatoid arthritis. Then the effects of lymphocytotoxic antibodies on killer T cells in cell-mediated lympholysis were investigated. The sera from patients with SLE and myasthenia gravis significantly suppressed cytolytic activity but those with rheumatoid arthritis showed no influence.
It was suggested that lymphocytotoxic antibodies in the patients with SLE, rheumatoid arthritis and myasthenia gravis were reactive preferentially with distinct T cell subsets.

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The present study was performed to disclose the abnormality of regulatory and cytotoxic T-cell system in myasthenic patients. T-cells from the patients usually suppressed immunoglobulin production. This suppressor activity was present in T_G-cell population. Some patients in early stage showed no suppressor activation even though there were immune complexes demonstrated in the sera, while in some progressed patients T_G suppressor cells were active but immune complexes were not detected. T_G-cells from some of the patients were cytotoxic to the target cells. This cytotoxicity seemed to be induced by immune complexes.
Activation by immune complexes of T_G-cells as suppressor is probably one of the nega tive feedback mechanisms to control the exess production of antibodies. It is very likely that such T_G-cell activation observed in myasthenic patients is response to autoantibody formation and indicates the presence of immune complexes. The patients who cannot elicite suppressor T-cells in the presence of immune complexes may have a defect in such regulatory mechanisms. The cytotoxicity caused by immune complexes and T_G-cells observed in myasthenic patients may play some roles in receptor injury especially in chronic changes of the tissue.

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Peripheral mononuclear cells from patients with systemic lupus erythematosus (SLE), when incubated for 48 hr with or without concanavalin A (ConA), were found to be capable of inhibiting the pokeweed mitogen (PWM)-induced polyclonal immunoglobulin (Ig) secretion by cells from normal individuals. Furthermore, these suppressor cells did not significantly affect on the Ig secretion by autologous B cells from patients with SLE. These results suggest that defective suppressive activity in patients with SLE is not at the T cell level, but, most likely, due to the defect of B cells in recognizing process of the suppressive information from suppressor T cells, caused by in vivo polyclonal B cell activation.

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Three cases of complete deficiency of the ninth component of complement (C9D) are described.
Case. 1-A 72-year-old male had a 10-year history of arthralgia in knees and fingers joints. He had been treated as rheumatoid arthritis (classical RA, stage III, class 2) with nonsteroid drugs. Clinical and serological features of the patient were completely compatible with RA except persistent hypocomplementemia.
Case. 2-A 25-year-old female had mild cervical lymphadenopathy but was otherwise well.
Case. 3-A 20-year-old female had a history of frequent erythema on extemities. Biopsy specimen of the skin showed no remarkable change.
They were not susceptible to infection. They showed low complement levels (CH50: 10-20.5U/ml vs normal 30-40) and undetectable C9 by both hemolytic and immunochemical assays. Since their sera had no anti-complementary activity and addition of purified C9 to their sera restored the hemolytic activities to normal levels, they were proved to have the complete deficiency of the ninth component of complement (C9D). The husband and one daugther of Case. 2 had half the normal C9 levels (heterozygous C9D) and another daugther showed no detectable C9 (homozygous C9D) who was healthy. These observations suggested an autosomal codominant type of the inhelitance for the C9 deficiency gene.

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