We have reported that the T-cells bearing receptors for Fc portion of IgG (Tγ cells) suppressed the growth of lymphoid cell line having Fc receptors in the presence of immune complexes (IC).
This phenomenon was tentatively named as “immune complexe dependent T-cell mediated cytotoxicity (IDTC)”. Further studies on the mechanisms of this phenomenon were described in this paper.
Presence of Fc receptors is necessory on both effector and target cells for cytotoxic effect to elicite, which suggested that effector cells act on target cells being bridged by IC via Fc receptors. When both cells were attached with IC independently, the phenomenon did not occur. This also indicated the necessity of bridging.
Growth of the target cells were inhibited by IDTC. However, this cytotoxic effect did not seem to be cytolytic.
Fractination of IC by polyethylenglycol density or ultracentrifugation indicated that active IC was of large molecular size more than 10⁶ dt.

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Bone marrow lymphocytes were studied on twenty healthy adults. Bone marrow lymphocytes were fractionated by BSA density gradient centrifuge. The population of bone marrow lymphocytes averaged as follows; E-RFC 8.9%, thymocyte-antigen positive cells 0.4%, Tγ 0.4%, Tμ 1.4%, SmIg⁺ cells 7.8%, EAC-RFC 11.7%, EA-RFC 6.2%, and K cells 2.8% respectively. About 80% of bone marrow lymphocytes were null lymphocytes. Bone marrow null lymphocytes were intermediate in size between small lymphocytes and lymphoblasts. Their nucleus contained no nucleolus and was leptochromatic. A lot of micro-villi was demonstrated on their surface membrane and their cytoplasma contained a few ribosomes and central dense bodies.
When bone marrow null cells were mixed lymphocyte cultured with allogeneic normal T lymphocytes and then stimulated with PWM, there appeared clg positive cells, indicating that bone marrow null cells could differentiate to the antibody producing cells under the regulation of T-cells by the antigenic stimulation.

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Using mixture of neuraminidase treated sheep erythrocytes (En) and zymosan-C3 complexes (ZC), simultaneous detection of T and B cells and monocytes were conducted in patients with malignant and non-malignant diseases and in healthy adults. In the mononuclear cells obtained by Ficoll-Conraydensity gradient centrifugation from peripheral blood of cancer bearing patients, marked increase inmonocytes differentiated by ingestion of ZC was found to be comparable with those of patients withnon-malignant diseases and healthy adults. On the other hand, the rate of T and B cells differentiatedby rosette formation with En or ZC showed a decrease in cancer-bearing patients.
Activity of peroxidase almost disappeared in large number of monocytes of healthy adults and patients with non-malignant diseases after ingestion of ZC particles while many peroxidase positive monocytesingesting ZC particles could be observed in cancer bearing patients.
An abnormality of the digestive system related to presence of foreign bodies in monocytes of cancerbearing patients is hypothesized.

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A case of a 29-year old female with systemic hupus erythematosus (SLE) complicating protein-losing enteropathy was reported.
She was admitted to our hospital on October 28, 1977, because of edema and diarrtea for 3 months. Physical examination on admission revealed facial and pretibial edema, pleural effusion and ascites. Laboratory examination showed hypoalbuminemia. The PVP test was 6.15% and the urine gave a negative test for protein. X-ray studies of the gastrointestinal tract were interpreted as within normal limits. A intestinal-biopsy specimen showed no specific changes. SLE was diagnosed by leukopenia, positive test for ANF, positive test for ADNA and low CH50 value in the serum. The specimen from a renal biopsy also supported the diagnosis. She was treated with prednisolone and a few months later, there were no recurrent signs and symptoms of SLE. Althogh the etiology of protein-losing enteropathy in SLE remains unknown, increasing capillary permiability may be the cause of the intestinal protein loss.

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Recently we have had an unusual case of primary macroglobulinemia associated with PIE syndrome and pruritic erythema. A 77-year-old woman was admitted to this hospital In February 1977, because of productive cough and subfebrile episodes of three years' duration. Her chest x-ray film showed linear and nodular shadow in the left lower lung field and infiltration in the right lower lung field. Elevated erythemas with itching sensation in both upper extremities and over the body were noted.
Investigations on admission were as follows; Bence Jones protein in the urine was negative. IgG level was 1, 300mg/dl, IgA 80mg/dl, and IgM 1, 400mg/dl. Electrophoretic picture of the serum showed monoclonal spike of IgM (κ) type. Cryoglobulin was negative. Cold agglutinin titer was within normal limits. Rheumatoid factor was positive, Mantoux reaction and DNCB negative. No osteolytic lesions were noted. Blood picture of peripheral blood as well as bone marrow showed eosinophilia with normal appearance, 34% and 14%, respectively. The bone marrow from the sternum showed lymphoid cells resembling plasma cells. These cells stained with FITC-labeled anti-μ, in which well-developed, somewhat dilated, rough endoplasmic reticulums were documented by electron microscopy. Biopsy specimens from pleura, cervical lymph node and cutaneous lesion revealed eosinophilic infiltrations with plasma cells.
We have discussed the combination of primary macroglobulinemia, PIE syndrome and erythema to investigate whether there is a pathogenetic relationship among the three. It should be considered that this combination can be pathogenetically related: (1) The eosinophilia of this case might be due to hypersensitivity reactions occurring in the presence of primary macroglobulinemia which is an immunodeficiency disease. (2) Host reaction against tumor cells might induce eosinophilia.

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A case of female patient of 64 years old with κ type IgG multiple myeloma was reported. She showed the positive anti-HBs antibody. Her IgG was fractionated by Na₂SO₄ precipitation and following DEAE columnchromatography. After the confirmation that the above fractionated IgG reacted with only anti-κ serum, her IgG fractions were digested with pepsin to obtain F (ab')₂ and Fc'. It has been demonstrated by the passive hemagglutination test that the F (ab')₂ fragments bind HBs antigens and Fc' fragment did not bind HBs antigens. Her suppressor T cells were markedly increasted.

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The effects of operation and a streptococcal immunopotentiator, OK-432, were evaluated on natural killer (NK) cell activity in 10 patients with malignant disease. Microassay methods were employed for a 5 hr-⁵¹Cr release test using mononuclear cells separated from peripheral blood and ⁵¹Cr-labeled K 562 cells as effector cells and target cells respectively with an effector-to-target ratio of 20: 1. The results are as follows: in each of 2 normal healthy donors, NK activity fluctuated from experiment to experiment and the levels of NK activity in one donor were almost always higher than in the other, suggesting that such fluctuation might occur in the process of NK assays. Thus the NK activities in cancer patients were corrected in each assay according to the control activities from the above healthy donors. In the patients with malignant disease, the corrected NK levels after operation were significantly lower in 3 out of 9 patients as compared with preoperative NK levels. When OK-432 was given for 12 consecutive days to each patient, cytotoxic activities of peripheral blood lymphocytes significantly increased in all patients, reached their peak on the 3rd day after administration and declined thereafter in most of the patients. Although the effector cells mediating the enhanced cytotoxic activity against K 562 are not identified yet, the above results suggest that OK-432 enhances NK cell activity in patients with malignant disease.

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