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Biomedical subjects

R N Taub

Publications and source records attributed to R N Taub.

At least 73 records · Page 4Linked to original sources
PubMed1976

Anergy to dinitrochlorobenzene and depression of T-lymphocytes in Crohn's disease and ulcerative colitis.

Skin reactivity to dinitrochlorobenzene (DNCB) and levels of circulating T-lymphocytes were measured in 15 patients with ulcerative colitis, 15 patients with Crohn's disease, and 12 normal control subjects. Diminished reactivity to DNCB was demonstrated in 87% of patients with Crohn's disease (P less than 0-001) and in 53% with ulcerative colitis (P less than 0-02), as compared with only 8-5% of controls; anergy was more frequent in Crohn's disease than in ulcerative colitis (P less than 0-05). Levels of circulating T-lymphoctes were also depressed in both Crohn's disease and ulcerative colitis (P less than 0-001) as compared with controls, with the values lower in Crohn's disease than in ulcerative colitis (P less than 0-02). There were no correlations of DNCB response with extent, duration, or severity of disease nor with T-cell levels within any patient group. These data provide further support for the concept that there is impairment of cell-mediated immunity among many patients with chronic inflammatory bowel disease, including both Crohn's disease and ulcerative colitis.

Colitis, Ulcerative↗
PubMed1976

Immunotherapy with dinitrochlorobenzene (DNCB) for recurrent squamous cell tumor of conjunctiva.

Over the course of nine years a young man sustained repeated recurrences of a squamous papillary epithelial tumor of the conjunctiva and canaliculus. Treatment had included repeated surgical excisions, fulguration, cryotherapy, and localized applications of Thiotepa. When we examined him in 1972 he had a recurrent lesion measuring about 1 cm in diameter. Because of past failures with the above-noted therapeutic modalities, we decided to treat him with immunotherapy using the immunological adjuvant DNCB (dinitrochlorobenzene). We sensitized him systemically to DNCB by applying 2,000 microng of this agent to the skin of his forearm. A spontaneous "flare" reaction, indicative of delayed hypersensitivity, developed. Delayed hypersensitivity to DNCB was confirmed by in vitro testing of his lymphocytes for their ability to produce migration inhibitory factor (MIF) in response to DNCB. Subsequent localized application of DNCB to the conjunctival tumor resulted in rapid regression of the lesion and there has been no recurrence during a follow-up period of three years. We believe this is the first time a conjunctival tumor has been successfully treated with immunotherapy.

Adjuvants, Immunologic↗
PubMed1976

Induction of secific immunological tolerance to histocompatible renal and skin allografts after donor strain spleen implantation.

Spleens from Lewis X BN F1 hybrid rats were directly anastamosed to the circulation of parental strain Lewis rats by a microvascular technique; no immunosuppressive drugs were given. Donor spleens enlarged massively during the first month after implantation, then grew gradually smaller over succeeding months without compromising their blood supply. Renal allografts were placed into bilaterally nephrectomised recipients that had already borne a splenic allograft for three months. The grafts functioned perfectly and showed no signs of rejection five months later. Donor LBN skin allografts transplanted to these animals showed markedly prolonged survival while third-party BUF rat skin allografts were rejected in first-set fashion. High titres of anti-LBN haemagglutinating antibody could be detected in the circulation of spleen-grafted animals during the first month; the titres fell to zero by the fourth month. Cellular reactivity of recipient cells against LBN antigens measured by the popliteal node GVH assay fell to minimal levels by the third month. These data indicate that the immune response to allografted tissues may be specifically and markedly suppressed in adult animals by continued presence of a donor-strain spleen.

Animals↗
PubMed1975

Antibody responses to leukemia-associated antigens during immunotherapy of chronic myelocytic leukemia.

We have studied immunologic reactivity to leukemia-associated antigens in patients with chronic myelocytic leukemia (CML) treated with chemotherapy and adjunctive immunotherapy. All patients were immunologically competent as measured by skin test reactivity to dinitrochlorobenzene. Immunotherapy consisted of allogeneic irradiated leukemic myeloblasts injected intradermally, with BCG vaccine (Research Foundation, Chicago, Ill.) given by multiple puncture at the same site. 10(9) cells plus BCG were given weekly for 4 wk, and 10(8) cells plus BCG were given at monthly intervals thereafter. Eight patients judged clinically to be in the stable phase of their disease developed circulating antibody against the immunizing blast cells demonstrable by cytotoxicity and immunofluorescence assays. The antibody also showed reactivity against a panel of myeloblasts (12 paients) but not against the corresponding remission lymphocytes (five patients) or normal lymphocytes (20 donors). In two cases the antibody showed reactivity against the patient's own leukemic blasts. Seven of these eight patients have maintained a steady clinical course ranging from 20 to 40 mo, while one entered the blastic phase and died. Six patients were judged to be in the aggressive phase of CML because of progressive leukocytosis and splenomegaly or increasing myeloblastosis; five died an average of 16 mo after diagnosis. Humoral antibodies were not detected in these patients after repeated courses of BCG and allogeneic leukemic cells. We conclude that specific active immunotherapy of patients with CML can abet the production of humoral antibody against blast cell antigens and that this response may be impaired during the aggressive phase of the disease.

Adult↗
PubMed1975

Inhibition of the graft-versus-host reaction. III. Altered in vivo distribution of spleen cells pretreated with Fab fragments of antithymocyte globulin.

51Cr-labeled parental strain spleen cells were pretreated in vitro with antithymocyte globulin (ATG) or Fab fragments of ATG before i.v. injection into F1 recipients. Recipients were killed at various intervals after injection and their organs were assayed for radioactivity in order to determine the in vivo distribution pattern of pretreated cells. 51Cr spleen cells pretreated with ATG were almost totally prevented from migrating to spleens, lymph nodes, bone marrow, Peyer's patches, lungs, and peripheral blood of recipients. Pretreatment of 51Cr spleen cells with noncytotoxic Fab of ATG also inhibited localization to these organs and tissues; however, the inhibition was not as complete as that of ATG-treated cells. Localization of Fab-treated 51Cr spleen cells to recipient nodes was inhibited to a greater extent than was localization to recipient spleens. There was no significant difference in the extent of inhibition of ATG-treated 51Cr spleen cells to recipient nodes and spleen. Organ counts from recipients killed at various intervals after injection of Fab-treated 51Cr spleen cells showed that Fab-treated cells do not recover their recirculating potential in vivo.

Animals↗
PubMed1974

Specificity of heteroantisera to human acute leukemia-associated antigens.

Antisera have been raised to human leukemic blast cells from individual patients in mice rendered tolerant with cyclophosphamide to remission leukocytes from the same individual. 10 antisera were raised against acute myelogenous leukemia (AML) cells and 5 antisera were raised against acute lymphoblastic leukemia (ALL) cells. Antisera to AML cells were absorbed with ALL cells, and antisera to ALL cells were absorbed with AML cells. Unabsorbed and absorbed antisera as well as antisera raised in nontolerant mice were tested for cytotoxicity against various cells of a panel containing myeloblasts from 35 patients with AML, lymphoblasts from 7 patients with ALL, myeloblasts from 7 patients with chronic myelogenous leukemia (CML) in blast crisis, peripheral blood leukocytes from 12 patients with acute leukemia in remission and 30 nonleukemic patients, and nucleated bone marrow cells from 10 nonleukemic patients. Unabsorbed antisera to AML or ALL cells raised in tolerant mice were highly cytotoxic to leukemic blasts cells but significantly less cytotoxic to remission and control cells. Antisera to AML cells absorbed with ALL cells retained measurable cytotoxicity against AML cells but were not cytotoxic to ALL cells or control cells. Similarly, antisera to ALL cells absorbed with AML cells retained significant cytotoxicity only to ALL cells. Control antisera raised in nontolerant mice were cytotoxic to all cells tested. Although species specific, histocompatibility, differentiation, maturation, and cell cycle-associated antigens may be responsible in part for the cytotoxic activity of the unabsorbed antisera, the absorbed antisera are probably detecting antigens specific for their leukemic cell type.

Animals↗