A significant decrease in natural killer (NK) activity of circulating mononuclear cells was demonstrated in 18 patients with aplastic anemia (AA). NK activity of normal control group in male showed its significant increase as compared with that in female. Whereas, no significant difference was observed between male and female patients. NK activity classified by the severity in Yamada's classification was reduced in the group of higher severity.
In review of NK activity classified by histological pictures on the bone marrow, no significant difference was observed among aplastic type, hypocellular type and normocellular type. In administration of steroid hormone in vivo to the patients with AA, no significant difference was observed on NK activity before and after the treatment. However, NK activity after treatment with hydrocortisone of peripheral mononuclear cells in vitro was significantly reduced in the pharmacologic concentration. In review of the viability after treatment with hydrocortisone by trypan blue dye exclusion test, hardly no reduction of viability was observed.
NK activity in the case removing the macrophage from the peripheral mononuclear cells showed no significnat difference as compared with that before removing the macrophage.
The abnormality not only of myelocytic, erythrocytic and megakariocytic system but also NK cell was suggested in the patients with AA.

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Correlation between serum inhibitory factor level and change of serum protein fractions was investigated in gastric cancer patients. The sera from normal donor and cancer patients were separated by Polyacrylamide gel slab electrophoresis with a gradient from 3 to 27%. In normal and cancer sera, thirty to fifty separated bands were presented on the gel. These bands were applied to Densitometory and serum protein patterns were drawn. Serum protein patterns were separated into 12 fractions, and calculated as pattern similarity. Changes of pattern similarity from cancer sera were markedly different from those from normal sera, and reflected the tumor advancing. Protein analysis by DEAE-cellulose colum chromatography and immunoelectrophoresis showed that Fractions 2, 3, and 8 were identified as α₁ acid glycoprotein, α₁ antitrypsin, and ceruloplasmin respectively. These protein fractions increased in accordance with the advance of the disease, and were thought to act as immunosuppressive factors. On the other hand, Fractions 6 and 7 were identified as transferrin and complement components respectively, and were thought to act as immunostimulatory factors. When the ratios of these two groups were investigated, refferring to as immunoregulatory ratio, immunoregulatory ratio from cancer sera decreased significantly with the advances of the disease.

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Classification of amyloidosis of these major proteins has been recently und ertaken. In our previous paper, we reported that immunoperoxidase method with anti-AA serum enabled us to identify protein AA even formalin fixed materials and its method was useful to make diagnosis of protein AA type of amyloidosis, so-called secondary amyloidosis. In this paper, we investigated protein AL derived from immunoglobulin light chain by the same method. We applied indirect immunoperoxidase method with anti-AA, anti-AL (κ), anti-AL (λ), anti-BJP (κ) and anti-BJP (λ) to 25 cases of amyloidosis and 14 cases of amyloidosis with plasma cell dyscrasia (PCD) consisting of primary amyloidosis and myeloma-associated one. The lattar was divided into three groups. Group 1 consisted four cases which presented kappa determinant inthe serum M-component and/or BJP (κ) in the urine. Group 2 included seven cases which presented lambda determinant in the serum M-component and/or BJP(λ) in the urine. Group 3 was three cases which were detected M-component neither in the serum nor in the urine.
(1) The most frequent underlying disease was found to be the rheumatoid arthritis in 16 out of 25 cases of secondary amyloidosis. All cases of secondary amyloidosis were sensitive to Congo red stain after treatment of potassium permanganate reaction (Wright's method) and were weakly to strongly positive by means of immunoperoxidase method with anti-AA. (2) All cases of amyloidosis with PCD were resistant by Wright's method. Regarding group 1, one of four was weakly positive by anti-AL (κ), but all were negative by anti-BJP (κ). Regarding group 2, one of seven was weakly positive by anti-AL (λ), but all were negative by anti-BJP (λ). Regarding group 3, all were negative by both anti-ALs and anti-BJPs.
Therefore, we would like to emphasize that immunoperoxidase method with anti-AA serumis quite desirable directly to identify protein AA. On the other hand, AL type amyloidosis was resistant by Wright's method and low frequency of positive cases by immunoperoxidase method with anti-AL sera. Our date suggest that making use of some kind of anti-AL sera for immunoperoxidase method enables us to identify protein AL in tissue sections.

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Functions of tumor cells from 5 cases of T cell malignancies (CLL: 3, malignant lymphoma: 1, malignant lymphoma with leukemic change: 1) were studied, in vitro with their conjunction to surface markers and clinical features.
In 3 out of 5 cases, tumor cell exerted either suppressor or helper function on MLR or Ig production of PWM stimulated lymphocyte.
In the patient (N. K) with CLL whose peripheral T cell suppressed 2 way MLR, PPD skin reaction was negative. Production of immunoglobulin by PWM stimulated normal lymphocyte, however, was not suppressed by the addition of his tumor cells to the culture, suggesting MLR and Ig production are independent immunological responce. By cytotoxic test, this tumor cell was proved to have surface markers characteristic to peripheral T lymphocyte (T₂).
In another patient (K. I.) with CLL, whose serum IgG was slightly increased (2194mg/dl), IgG production by normal lymphocytes in vitro was enhanced by addition of tumor cells. It may well be therefore, considered that the tumor cells were derived from helper cell origin. Although helper cell has been considered to be Tr negative, most of the tumor cells of this patient were Tr (EA rosett) and T₂ positive.
The third case of functioning T cell malignancy (patient F. N.) was malignant lymphoma (diffuse, medium-sized cell type). Tumor cells prepared from lymphonodes clearly suppressed both MLR and Ig production in vitro. Clinical feature reflexed well the above bindings, namely PPD skin reaction was negative and serum IgG concentration was extremely low (450mg/dl). This tumor cell was also Tr and T₂ positive.

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Circulating immune complex (IC) was detected by means of the 3.5% polyethylene glycol (PEG, MW 6, 000) precipitation method, in the plasma of 36 patients with acute Kawasaki disease. When compared to control plasma, the results showed a significant increase of IC. IC was isolated in gathered plasma sample from 36 patients. When this IC was added to normal PWM-stimulated lymphocyte culture, production of plaque forming cells (PFC) was found to be suppressed. It was also shown that normal lymphocytes, after having been exposed to the patient IC, were capable of exerting inhibitory activity on PFC response of the autologous Iymphocytes to PWM. Furthemlore, IgG-IC and IgM-IC were prepared from the patient IC according to a technique using ion-exchange chromatography on DE-52 cellulose. Then, normal T cells, which were separated by SRBC rosetting technique, were incubated with IgG-IC or IgM-IC for 24 hours. After incubation, these T cells were added to the PWM-stimulated autologous B cell culture. It was demonstrated that preincubation of normal T cells with the IgG-IC or IgM-IC inhibited the autologous B cell response to PWM. When these IgG-IC or IgM-IC treated T cells were irradiated by 2, 000rad, the inhibitory activity was abrogated. Therefore, suppressor T cells may be induced not only by the IgG-IC, but also by the IgM-IC.

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This patient was a 16-year-old girl who was diagnosed as a systemic lupus erythematosus (SLE)/progressive systemic sclerosis (PSS) overlap syndrome with 8 year history.
She was in good health until 1970, when she noticed subcutaneous bleeding. The diagnosis of idiopathic thrombocytopenic purpura was made and she was treated with corticostreoids. In 1973, butterfly rash, polyarthritis, hemolytic anemia and LE cells phenomenon developed and she was diagnosed as SLE. In 1975, sclerodermatous skin changes with Raynaud's phenomenon developed. The area of sclerosis was rapidly spread from her fingers to the trunk and she was diagnosed as PSS besides SLE. In 1979, she admitted to Keio university hospital because proteiuria, which has appeared since 1977, developed to nephrotic syndrome. On the labolatory examinations, a skin biopsy showed an atrophy of the epidermis and a proliferation of collagen fibers in the dermis. The deposition of IgM at the dermal-epidermal junction was found. A renal biopsy demonstrated wire-loop lesions. In the serum from this patient, many autoantibodies, anti-RNP, anti-Sm, anti-Og (Scl₇₀) and anti-ds DNA antibodies, were found. circulating immune complexes were also detected in the serum by Raji cell assay.
In summary, this patient had a typical SLE/PSS overlap syndrome and had autoantibodies specific for both SLE and PSS. Circulating immune complexes and immune complex nephritis were present in this rare case.

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Granulocyte functions were studied in a case of Wiskott-Aldrich syndrome. In the agarose plate, granulocytes of this patient were shown to have moderately decreased responses in chemotaxis induced by N-formyl-methionyl-leucyl-phenylalanine (FMLP) and zymosanactiv-ated human serum (ZAS), whereas they were shown to have a normal capacity of random migration. Phagocytosis and superoxide production by neutrophils were within normal limits. Chemotaxis of neutrophils in this patient was improved by transfer factor therapy. Clinical improvement of patients with Wiskott-Aldrich syndrome treated by transfer factor may be due to recovery of granulocyte functions.

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