Kidney transplantation in the inbred rat preimmunized with donor strain spleen cells.
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Biomedical subjects
Publications and source records attributed to T Natori.
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The immune response to bovine insulin (BI) in the rat is controlled by the major histocompatibility complex (Mhc)-linked immune response gene (Ir-BI) and immune suppression gene (Is-BI). In the present study, we investigated the low responsiveness to BI in the WKAH rat (RT1k) and attempted to explore the functional link between Is-BI and Mhc class II molecules. Lymph node cells (LNC) from the low responder (WKAH) rats responded well to BI when a large amount of antigen was added to the culture in vitro or after OX8-bearing (OX8+) T cells were eliminated. These LNC, after the elimination of OX8+ cells, could show the RT1.Dk-restricted proliferative response upon in vitro challenge with BI, BI-B chain, or pork insulin. In addition, OX8+ T cells, which were activated with BI and antigen-presenting cells (APC) in vitro, suppressed the anti-BI response of W3/25-bearing proliferating T cells from BI-immunized rats. The results have demonstrated that proliferating T-cell repertoires do exist to BI, which recognize BI-B chain in the context of RT1.Dk molecules in the WKAH rat, and that the state of low responsiveness is mediated to a great extent by antigen-specific OX8+ suppressor T (Ts) cells. Furthermore, the elimination of APC or the addition to RT1.Bk-specific monoclonal antibody in the in vitro secondary activation culture of Ts cells diminished the suppressive activity of OX8+ Ts cells. In the induction phase of Ts cells it therefore seems to be necessary for these cells to recognize BI together with RT1.Bk molecules on APC.
A rare case of recurrent cervical cancer presenting multiple metastases to the small intestine is reported. A 69-year-old Japanese woman with a past history of early-stage (Ia) cervical cancer 13 years previously suffered sudden onset of panperitonitis caused by perforation of the small intestine. In the perforated lesion, squamous cell carcinoma, which was histologically similar to that of the primary lesion, was observed, and was diagnosed as a late recurrence of the cervical cancer. Perforation of the small intestine caused by tumor metastasis, especially metastasis from cervical cancer, rerely occurs. Furthermore, recurrence of an early cervical cancer presenting 13 years after hysterectomy is extremely rare. The present case draws attention to the possibility of late recurrence of cervical cancer, even in cases treated at the early-stage.
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Primary malignant lymphoma of gastrointestinal tract is relatively rare and the most of it are seen in stomach or small intestine, and in Japan only 130 cases of primary large intestinal malignant lymphoma were reported from the accumulating results of the postoperative cases in the 11th Congress of the Japanese Research Society for Cancer of the Colon and Rectum. This paper describes the case report of the primary malignant lymphoma originated from the cecum, and the review of the literature. The patient was 63 year-old female, who came to this hospital for slight fever and right lower abdominal pain that was gradually increasing. After the investigation by using barium enema and the intrapelvic CT, cecum tumor was detected. The ileocecal excision was performed, and revealed the 4 X 4.5 cm tumorous type lesion of which surface was slightly irregular. Histopathologically the tumor was follicular lymphoma (partial type), medium sized cell type by the Lymphoma-leukemia Study Group (LSG) classification. After discharge, cyclophosphamide was administered by 100 mg/day for six weeks, and the sign of the recurrence has not been observed.
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Serological, functional, and chemical analyses of murine class II antigens were performed using a unique monoclonal antibody, 1E4, which was obtained from a rat-mouse hybridoma. 1E4, which is specific for a monomorphic determinant on HLA-DR antigens in humans and a polymorphic determinant on RT1-Da antigens in rats, detected class II antigens on the cells from mice carrying H-2 haplotypes of b, d, p, q, u, v, k, j, r, but not those with f or s haplotypes. Analysis of two-dimensional gel electrophoresis revealed that 1E4 monoclonal antibody recognized at least Ek/b, d, k and Ab, d molecules. 1E4 blocked the T cell proliferative responses to beef insulin and TGAL in B10 and BALB/c mice, as well as proliferative responses to GLT in BALB/c mice and to PPD in C3H/He mice, as had been demonstrated in other species. Furthermore 1E4 inhibited MLR to stimulator cells that expressed Ab, d or Ek/b, k, d molecules. Taken together, these findings indicate that an epitope detected by 1E4 on class II antigens has been well preserved across species barriers. This epitope may play a major role or be closely related to the functional site that is involved in recognition of nominal antigens by T cells.
Leukocyte subsets that infiltrated into unmodified LEJ(RT1j)2 liver grafts from WKAH(RT1k) hosts were studied. This strain combination is fully allogeneic and yields acute rejections in skin and kidney transplantations. On days 3, 7, and 14, cellular infiltrates gradually increased, and many hepatocytes were degenerative and lost cellular glycogen. Blastoid lymphocytes were frequently seen, and mitotic features of hepatocytes were prominent (on day 14, 3 to 4/10 high-power fields). Later, on days 30, 50, and 300, the cellular infiltrates gradually subsided, and blastoid lymphocytes were rarely seen. Throughout the course, Ia+ cells (RT1.Dk+ and/or RT1.B+ cells) were the major cell populations infiltrating into the grafts. Most of the host RT1.D+ cells were histiocytoid in appearance on immunoelectron microscopy. Histiocytoid cells were the most numerous infiltrating cells, constituting 30-50% of the total infiltrating cells. There were different distributions of T cell subsets between the portal and sinusoidal areas, as we previously observed in acutely rejected rat renal allografts. Both RLyt-1+,2-(Th) and RLyt-1+,2+(Tc/s) cells were found almost equally in the portal area, while RLyt-1+,2+(Tc/s) cells predominated over RLyt-1+,2-(Th) cells in the sinusoidal area. However, a gradual replacement of RLyt-1+,2-(Th) cells by RLyt-1+,2+(Tc/s) cells, as seen in the perivascular area of renal grafts, was not found in the portal areas of the liver grafts. Except for the latter finding, the pattern of cellular infiltrates was similar to that of acute renal rejection, and the significance of these cellular infiltrates is discussed.
The lymph node cells from 11 strains of rats, differing in the genotype of the major histocompatibility complex of the rat (RT1), were examined on the basis of their proliferative response to the cell wall antigen of Streptococcus mutans. The 11 rat strains fell into three groups: high, intermediate, and low responders. To demonstrate the influence of the major histocompatibility complex on immune responsiveness to S. mutans, further experiments were performed using the RT1-congenic rat strains WKAH.1L(LEW), WKAH. 1AV1(ACI), and WKAH.1J(LEJ), which differ only in the genotype of the RT1 region. Although the background genes of each strain were of WKAH origin, WKAH.1L(LEW) and WKAH.1AV1(ACI) rats showed a low response whereas WKAH.1J(LEJ) rats showed a moderate response to the S. mutans cell wall antigen. The results indicate that the immune response is controlled by the class II gene(s) in RT1. Furthermore, the RT1.D locus products were shown to play an important role in the restriction molecule, since a monoclonal antibody, HOK7, directed to the RT1.Dk locus products reduced the proliferative response of lymph node cells.
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The immune responsiveness to MLM bacilli is investigated using secondary T-cell proliferative response to sol. MLM in B10 mice with macrophages from various B10 congenic strains of mice. The results show that T cells of B10 mice are able to respond with macrophages from B10 or B10A(5R) mice, but not with those from B10A, B10A(4R), and B10BR mice. In addition, the proliferative response to sol. MLM of B10 spleen cells was suppressed by adding an anti-I-Ab monoclonal antibody into the culture. Thus, the results indicate that the immune response to sol. MLM is restricted by I-Ab gene products. In terms of the weight of lepromas, and of the number of MLM bacilli in the spleen and liver, B10A, B10A(4R), and B10BR mice appeared to be susceptible to MLM bacilli (low responders). The macrophages obtained from the low-responder mice had a significantly lower phagocytic activity than those from high-responder mice (r = 0.967). The high-responder mice were inversely associated with the weight of lepromas (r = 0.731). These results suggest that the high phagocytic activity of B10 or B10A(5R) macrophages triggers an effective antigen presentation to helper T cells being restricted by I-Ab molecules, which could account for the immune resistance to MLM bacilli in B10 or B10A(5R) mice.
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