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228 results on '"Mordes, J P"'

4. Costimulation and Autoimmune Diabetes in BB Rats

Author

Beaudette-Zlatanova, B. C., Whalen, B., Zipris, D., Yagita, H., Rozing, J., Groen, H., Benjamin, C. D., Hunig, T., Drexhage, H. A., Ansari, M. J., Leif, J., Mordes, J. P., Greiner, D. L., Sayegh, M. H., and Rossini, A. A.

Published
2006

36. BB rat thymocytes cultured in the presence of islets lose their ability to transfer autoimmune diabetes.

Author

Whalen, Barbara J., Marounek, Jan, Weiser, Peter, Appel, Michael C., Greiner, Dale L., Mordes, John P., Rossini, Aldo A., Whalen, B J, Marounek, J, Weiser, P, Appel, M C, Greiner, D L, Mordes, J P, and Rossini, A A

Subjects
ANTIGENS, THYMUS, ORGAN culture, ANIMAL experimentation, CELL culture, CELL receptors, COMPARATIVE studies, RED blood cell transfusion, HOMOGRAFTS, IMMUNITY, IMMUNIZATION, IMMUNOPHENOTYPING, TYPE 1 diabetes, INTERFERONS, INTERLEUKINS, ISLANDS of Langerhans, LYMPH nodes, RESEARCH methodology, MEDICAL cooperation, RATS, RESEARCH, SPLEEN, T cells, TIME, TISSUE culture, EVALUATION research
Abstract

Thymocytes from adult BB rats can adoptively transfer autoimmune diabetes to athymic recipients. It is also known that the development of BB rat T-cells is recapitulated in adult thymus organ cultures (ATOCs). Based on these observations, we tested the hypothesis that cells capable of the adoptive transfer of diabetes would be present in long-term ATOCs but could be rendered nondiabetogenic by co-culture with appropriate antigens. We observed that cells recovered from adult diabetes-resistant BB (BBDR) rat thymi cultured for up to 14 days can adoptively transfer disease to athymic WAG-rnu/rnu rats treated with polyinosinic: polycytidylic acid and a monoclonal antibody to preclude development of ART2a+ regulatory T-cells. Co-culture of adult BBDR thymi in the presence of BBDR thyrocytes had no effect on the ability of recovered cells to induce diabetes in 70-80% of adoptive recipients. In contrast, co-culture in the presence of islets prevented transfer of diabetes, on average, in >90% of recipients. Fresh islets, frozen islets, and islets pretreated with streptozotocin to deplete insulin were equally effective in preventing diabetes, but none prevented insulitis in nondiabetic recipients. Co-culture in the presence of islets was not associated with detectable alterations in phenotype or in the secretion of gamma-interferon or interleukin-4, either in cultures or in cells recovered from adoptive recipients. We conclude that islet antigens involved in the initiation of autoimmune diabetes in BB rats may be absent or deficient in BB rat thymi. Exposure of ATOCs to exogenous islets may lead to deletion or anergy of diabetogenic T-cells or to the positive selection of regulatory T-cells. [ABSTRACT FROM AUTHOR]

Published
2001
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37. Prolonged survival of rat islet and skin xenografts in mice treated with donor splenocytes and anti-CD154 monoclonal antibody.

Author

Gordon, Ethel J., Markees, Thomas G., Phillips, Nancy E., Noelle, Randolph J., Shultz, Leonard D., Mordes, John P., Rossini, Aldo A., Greiner, Dale L., Gordon, E J, Markees, T G, Phillips, N E, Noelle, R J, Shultz, L D, Mordes, J P, Rossini, A A, and Greiner, D L

Subjects
XENOGRAFTS, SPLEEN, MONOCLONAL antibodies, CYTOLOGY, PHYSIOLOGY
Abstract

Treatment of C57BL/6 mice with one transfusion of BALB/c spleen cells and a brief course of anti-CD154 (anti-CD40 ligand) antibody permits BALB/c islet grafts to survive indefinitely and BALB/c skin grafts to survive for approximately 50 days without further intervention. We now report adaptation of this protocol to the transplantation of islet and skin xenografts. We observed prolonged survival of rat islet xenografts in mice treated with donor-specific spleen cell transfusion and anti-CD154 monoclonal antibody (mAb). Challenge islet xenografts placed on these animals indicated that graft acceptance was species-specific but not strain specific. Spleen cells from recipients bearing intact grafts led to rejection of rat islet xenografts in scid mice, suggesting that graft acceptance was not due to complete clonal deletion of xenoreactive cells. We also observed prolonged survival of rat skin xenografts in mice treated with donor-specific transfusion and anti-CD154 mAb. Prolonged survival of skin xenografts was also species specific. We conclude that treatment with appropriately timed donor-specific transfusion and anti-CD154 mAb induces durable survival of both islet and skin xenografts in mice. Because this procedure is targeted directly at CD154, a co-activation molecule expressed predominantly by activated CD4+ T-cells, the results suggest that CD4+ cells have a major role in the cellular immune response to xenografts. [ABSTRACT FROM AUTHOR]

Published
1998
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44. Requirement of the JIP1 scaffold protein for stress-induced JNK activation.

Author

Whitmarsh, A J, Kuan, C Y, Kennedy, N J, Kelkar, N, Haydar, T F, Mordes, J P, Appel, M, Rossini, A A, Jones, S N, Flavell, R A, Rakic, P, and Davis, R J

Abstract

The c-Jun N-terminal kinase (JNK) signal transduction pathway is activated in response to the exposure of cells to environmental stress. Components of the JNK signaling pathway interact with the JIP1 scaffold protein. JIP1 is located in the neurites of primary hippocampal neurons. However, in response to stress, JIP1 accumulates in the soma together with activated JNK and phosphorylated c-Jun. Disruption of the Jip1 gene in mice by homologous recombination prevented JNK activation caused by exposure to excitotoxic stress and anoxic stress in vivo and in vitro. These data show that the JIP1 scaffold protein is a critical component of a MAP-kinase signal transduction pathway.

Published
2001
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45. Characterization of mouse Rt6.1 NAD:arginine ADP-ribosyltransferase.

Author

Moss, J, Stevens, L A, Cavanaugh, E, Okazaki, I J, Bortell, R, Kanaitsuka, T, Mordes, J P, Greiner, D L, and Rossini, A A

Abstract

Rat RT6 proteins, and perhaps mouse Rt6, identify a set of immunoregulatory T lymphocytes. Rat RT6.1 (RT6.1) and rat RT6.2 (RT6. 2) are NAD glycohydrolases, which catalyze auto-ADP-ribosylation, but not ADP-ribosylation of exogenous proteins. Mouse Rt6.1 (mRt6.1) also catalyzes auto-ADP-ribosylation. The activity of mouse cytotoxic T lymphocytes is reportedly inhibited by ADP-ribosylation of surface proteins, raising the possibility that mRt6 may participate in this process. The reactions catalyzed by mRt6, would, however, need to be more diverse than those of the rat homologues and include the ADP-ribosylation of acceptors other than itself. To test this hypothesis, mRt6.1 and rat RT6.2 were synthesized in Sf9 insect cells and rat mammary adenocarcinoma (NMU) cells. mRt6.1, but not rat RT6.2, catalyzed the ADP-ribosylation of guanidino-containing compounds (e.g. agmatine). Unlike RT6.2, mRt6.1 was a weak NAD glycohydrolase. In the presence of agmatine, however, the ratio of [adenine-14C]ADP-ribosylagmatine formation from [adenine-14C]NAD to [carbonyl-14C]nicotinamide formation from [carbonyl-14C]NAD was approximately 1.0, demonstrating that mRt6.1 is primarily a transferase. ADP-ribosylarginine hydrolase, which preferentially hydrolyzes the alpha-anomer of ADP-ribosylarginine, released [U-14C]arginine from ADP-ribosyl[U-14C]arginine synthesized by mRT6.1, consistent with the conclusion that mRt6.1 catalyzes a stereospecific Sn2-like reaction. Thus, mRt6.1 is an NAD:arginine ADP-ribosyltransferase capable of catalyzing a multiple turnover, stereospecific Sn2-like reaction.

Published
1997

46. Depletion of RT6.1+ T lymphocytes induces diabetes in resistant biobreeding/Worcester (BB/W) rats.

Author

Greiner, D L, Mordes, J P, Handler, E S, Angelillo, M, Nakamura, N, and Rossini, A A

Abstract

To investigate the role of RT6+ T cells in the pathogenesis of diabetes in BB/W rats, we treated animals from the diabetes-resistant (DR) subline with anti-RT6.1 lymphocytotoxic mAb. This depleted greater than 95% of peripheral RT6+ T cells but did not substantially reduce levels of circulating T cells or the in vitro response of spleen cells to mitogen. Treatment of 30-d-old DR BB/W rats in this way: induced insulitis and diabetes, rendered nondiabetic RT6-depleted DR rats susceptible to the adoptive transfer of diabetes by spleen cells from acutely diabetic BB/W rats, and yielded DR spleen cell populations capable of the adoptive transfer of diabetes to diabetes-prone (DP) or DR recipients. Treatment of DR rats beginning at 60 d of age failed to produce these effects. These results suggest that both susceptibility and resistance to diabetes in the BB/W rat are in part regulated by the RT6+ T cell subset and provide evidence for the importance of regulatory T lymphocytes in the pathogenesis of autoimmunity and diabetes in BB/W rats.

Published
1987
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47. Transfusions enriched for W3/25+helper/inducer T lymphocytes prevent spontaneous diabetes in the BB/W rat

Author

Mordes, J., Gallina, D., Handler, E., Greiner, D., Nakamura, N., Pelletier, A., and Rossini, A.

Abstract

Transfusions of spleen cells are known to prevent spontaneous autoimmune diabetes in susceptible BB/W rats, while T cell-depleted transfusions are ineffective. To characterize further the protective cell(s), we transfused young diabetes prone rats with splenocytes from diabetes resistant BB/W rats that were treated in vitro to enrich them in either OX8+(suppressor/cytotoxic) T cells or W3/25+(helper/inducer) T cells. Diabetes subsequently occurred in 19 of 29 (66%) recipients of OX8-enriched, W3/25-depleted cells and 20 of 37 (54%) controls, but in only 7 of 30 (23%) recipients of W3/25-enriched, OX8-depleted cells (p<0.005). Transfusion of spleen cells from diabetes resistant donor rats pretreated in vivo to deplete OX8+cells also prevented diabetes in susceptible BB/W recipients. We conclude that transfusions of W3/25+helper/inducer splenic T lymphocytes obtained from diabetes resistant animals prevent spontaneous diabetes in the BB/W rat.

Published
1987
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