γδT lymphocytes, which are CP 3+ lymphocytes that express γδ chains of the T-cell antigen receptor (TCR) on their surface, are functionally distinct from αβT lymphocytes, which express αβ chains of the TCR. γδT lymphocytes are thought to differentiate in mouse hepatic sinusoids, to play a role in antitumor action, and to act as natural killer cells. The purpose of this study was to examine whether γδT lymphocytes in the peripheral blood are suppressed when hepatic sinusoids are damaged during transcatheter arterial embolization (TAE). The numbers of αβT lymphocytes and γδT lymphocytes in the peripheral blood were examined with monoclonal antibodies and flow cytometry before and after TAE in 32 patients (from 46 to 78 years of age) with liver cirrhosis and hepatocellular carcinoma. The number of αβT lymphocytes before and after TAE was unchanged. However, the number of γδT lymphocytes and the ratio of γδT lymphocytes to CD 3 +lymphocytes were significantly decreased for 3 weeks after TAE treatment. This decrease suggests that TAE suppresses the supply of γδT lymphocytes to the peripheral blood. In addition, TAE may weaken a patient's antitumor immunity, because γδT lymphocytes that have antitumor activity decrease after TAE.

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A study was conducted to clarify the mechanism of donor specific immunological unresponsiveness in renal transplant recipients with a well functioning kidney, since this might provide a clue to the nature of donor specific immunosuppression. Peripheral blood lymphocytes (PBL) were obtained from three renal transplant recipients, the donors (mother), the fathers and healthy volunteers as 3rd party and used in the present study. PBL from one of the three renal transplant recipients, which were donor specific unresponsive in MLR (Mixed Lymphocyte Reaction) and CML (Cell Mediated Lympholysis), suppressed the MLR, CML and synthesis of IL-2 from 3rd party PBL in a double chamber assay only when stimulated by the donor PBL. This suppression was abolished by the treatment with CD 3 or CD 8 antibodies and complement. RT-PCR was performed to investigate the suppressive effect of the recipient's PBL on IL-2 mRNA expression. In the double chamber MLR, expression of IL-2 mRNA by the PBL from 3rd party was also suppressed only when the recipient's PBL were stimulated by the donor PBL. These results indicate that one of the mechanisms responsible for donor specific immunological unresponsiveness is the presence of donor specific suppressor T cells in recipient's PBL and that these cells project suppressive effect on lymphocytes by producing a humoral suppressive factor (s) that suppress the expression of the IL-2 mRNA only when stimulated by donor PBL.

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An autopsy case of rheumatoid arthritis (RA) with acute exacerbation of interstitial pneumonia is reported.
A 57-year-old woman with longstanding RA was admitted to our hospital because of progressive dyspnea. On chest roentogenogram, diffuse interstitial shadow was confirmed in both lungs. Chest computed tomography (CT) showed difffuse lesion of elevated density of CT level in both lung. She was diagnosed as an acute exacerbation of interstitial pneumonia, and treated by methylpredonisolone pulse therapy (1, 000mg/day). Although cyclosporin A (2mg/kg/day) was combined to steroid therapy, she was died of progressive respiratory failure. The histological findings of the lung showed extensive fibrosis with alveolar damage associated with hyaline membranes, edema and hemorrhage in alveolar space.

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We reported a case of primary macroglobulinemia with stomach and pulmonary invasion. The patient was 71 years-old who had cervical lymphadenopathy and abdominal pain. Biopsy material of cervical lymph node showed non-Hodgkin's lymphoma, and he was diagnosed primary macroglobulinemia by IgM immunological histo-chemical staining of materials of stomach biopsies. Combination chemotherapies were not effective for the reduction of IgM-λ protein, and organ invasion seemed to be progressive, so we tried interferon-α (IFN-α) to control M component. Daily injection of 6 megaunits of IFN-α induced significant reduction of M component and pulmonary invasion. This favorable changes were observed for 1 year. However, his pulmonary invasion on X-ray films relapsed and he died of respiratory failure by reason of severe pneumonia. IFN-α is currently available for myeloproliferative disease, especially chronic myelogenous leukemia and multiple myeloma. This case report showed that IFN-α was also available for primary macroglobulinemia.

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