国立療養所邑久光明園において,1962年から1971までと,1977年から1987年までに行われた225例の剖検例の中で,各々の期間に3例ずつ,計6例の悪性リンパ腫を経験した。性別はすべて男性で,平均年齢は63歳であった。病型は,4例はらい腫型,残りの2例は境界群と類結核型であった。3例は頚部から,3例は後腹膜から発生した。免疫組織化学染色では6例ともB細胞由来と同定された。発生頻度は2.66%であり,特に高くはないが,6例中4例はらい腫型であり,残りの2例は境界群と類結核型であることは,らい患者における悪性リンパ腫の発生は,らい腫らいにおける細胞性免疫抑制状態と加令とに深く関係していると考えられる。我国のらい療養所では高齢化が急速に進んでいるので,今後,高齢のらい腫らい患者の悪性リンパ腫の発生は増加すると思われる。

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Splenic macrophages induced by intravenous injection of Mycobacterium leprae vaccine (ML-vaccine) consisting of heat-killed M. leprae (HK-ML; 6×108/ml) and live M. bovis BCG (10mg/ml) were studied for their suppressive activity against lymphoproliferative response to concanavalin A (Con A). Spleen cells (SPCs) of host mice received 0.1ml of the vaccine 2weeks before harvest showed markedly reduced Con A mitogenic response. Such phenomenon was seen also in the case of mice which were given live BCG (1mg) alone, but was not in the case of injection with HK-ML (6×107) alone. When splenic macrophages which were cultivated on a microtiter well for a monolayer culture was studied for the suppressive activity against Con A mitogenic response to splenic T cells, potent suppressive activity was found in mice treated with ML-vaccine as well as live BCG alone, but not in mice given HK-ML alone. Activity of the suppresssor macrophages per spleen in ML-vaccine-treated mice was nearly the same as in mice given BCG alone. However, the suppressor activity per individual macrophage was considerably higher in ML-vaccine-treated mice than in the case of BCG-injected mice. The two macrophages produced almost the same intensity of chemiluminescence in response to triggering by phorbol myristate acetate, and thereby, indicating that they were activated in a similar level. When resident peritoneal macrophages with a weak suppressive activity against lymphoproliferative response were incubated in the presence of ML-vaccine, their suppressor activities were markedly augmented. The same phenomenon was also noted when the macrophages were treated with HK-ML, but the efficacy was much lower than that of ML-vaccine. These results indicate that the suppressor macrophage-inducing ability of ML-vaccine consisting of HKML and live BCG is mainly attributable to the latter component.

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Ultrathin sections of nerves of tuberculoid and lepromatous leprosy were examined in an electron microscope for changes in endoneural blood vessels. In the tuberculoid nerves, hypertrophy of endothelial cells was the most prominent feature. This was to such an extent that the lumen of blood vessel was often closed. Endoneural blood vessels showed multilayers seperated by collagen and ground substances. In contrast, in the lepromatous nerves, there was no hypertrophy of endothelial cells in the blood vessels and the lumen of the vessels was open. M. leprae were seen within the endothelial cells and these organisms were intact and probably viable. These observations suggest a possible involvement of endoneural blood vessels which may contribute to nerve damage in leprosy.

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The characteristics of the cells of mononuclear phagocyte series (MPS) in the dermal granulomas of tuberculoid and lepromatous leprosy were studied by elereron microscopy. In the tuberculoid granulomas, majority of the cells of MPS (epithelioid cells) showed a distinct appearence. They were seen in close association with a large number of activated lymphocytes. The cells of MPS had a prominent nucleus. Their cytoplasm contained mainly rough endoplasmic reticulum, developed golgi and was free of M. leprae or its products. In contrast, the cells of MPS (macrophages) in lepromatous leprosy had a large nucleus. Their cytoplasm contained mainly whole M. leprae organisms/its phagocytosed products and rough endoplasmic reticulum. There was paucity of lymphocytes in these granulomas. These observations support the view that the cells of MPS in the tuberculoid granulomas may be secretory while those in the lepromatous granulomas were phagocytic.

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らい菌液またはレプロミンおよびPGL-1によって,L型患者の末しょう血リンパ球のConA応答の抑制がみられる。らい菌液またはレプロミンによっては,サプレッサーT細胞が誘導されるためであるとMehra等により証明されてきた。しかし,PGL-1による免疫抑制がどのような機作により誘導されるかについては明らかにされていない。我々は,マウスの系を用いる事により,PGL-1によるConA応答抑制機作の解析をおこなった。
結果,PGL-1投与(in vivoまたはin vitro)により,マウスの細胞性免疫低下がみられた。即ち1)対照マウスの脾細胞は,PGL-1投与(in vitro 40μg/mlによりCon A or PHA反応の低下を示した。2) PGL-1静注マウスの脾細胞は,これらマイトーゲン反応の低下を示し,これらの低下は,新鮮マウス腹くう内マクロファージの投与により回復した。この際,PGL-1投与マウス脾細胞による対照マウス脾細胞の反応の抑制は見られず,PGL-1投与マウス脾細胞が,抑制性因子を産生していないことを示している。これらのことから,PGL-1投与による抑制は,マクロファージによる機能障害によると考えられる。

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