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Institution

University of Medicine and Dentistry of New Jersey

Education
About: University of Medicine and Dentistry of New Jersey is a based out in . It is known for research contribution in the topics: Population & Poison control. The organization has 14634 authors who have published 19610 publications receiving 1041794 citations.


Papers
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Journal ArticleDOI
TL;DR: The selective expression of TECK and GPR-9-6 in thymus and small intestine implies a dual role for GPR/CCR-9, both in T cell development and the mucosal immune response, and proposes the designation CCR-9 for this chemokine receptor.
Abstract: TECK (thymus-expressed chemokine), a recently described CC chemokine expressed in thymus and small intestine, was found to mediate chemotaxis of human G protein–coupled receptor GPR-9-6/L1.2 transfectants. This activity was blocked by anti–GPR-9-6 monoclonal antibody (mAb) 3C3. GPR-9-6 is expressed on a subset of memory α4β7high intestinal trafficking CD4 and CD8 lymphocytes. In addition, all intestinal lamina propria and intraepithelial lymphocytes express GPR-9-6. In contrast, GPR-9-6 is not displayed on cutaneous lymphocyte antigen–positive (CLA+) memory CD4 and CD8 lymphocytes, which traffic to skin inflammatory sites, or on other systemic α4β7−CLA− memory CD4/CD8 lymphocytes. The majority of thymocytes also express GPR-9-6, but natural killer cells, monocytes, eosinophils, basophils, and neutrophils are GPR-9-6 negative. Transcripts of GPR-9-6 and TECK are present in both small intestine and thymus. Importantly, the expression profile of GPR-9-6 correlates with migration to TECK of blood T lymphocytes and thymocytes. As migration of these cells is blocked by anti–GPR-9-6 mAb 3C3, we conclude that GPR-9-6 is the principal chemokine receptor for TECK. In agreement with the nomenclature rules for chemokine receptors, we propose the designation CCR-9 for GPR-9-6. The selective expression of TECK and GPR-9-6 in thymus and small intestine implies a dual role for GPR-9-6/CCR-9, both in T cell development and the mucosal immune response.

515 citations

Journal ArticleDOI
TL;DR: It is reported that in humans, the 600 kDa RNF20/40 complex is the E3 ligase and UbcH6 is the ubiquitin E2-conjugating enzyme for H2B-Lys120 monoubiquitination, and the hPAF complex is recruited to transcriptionally active genes in vivo.

515 citations

Journal ArticleDOI
TL;DR: The ego-1 gene is the first example of a gene encoding an RdRP-related protein with an essential developmental function, and a protein required for germ-line development in C. elegans may be a component of the RNA interference/PTGS machinery.

515 citations

Journal ArticleDOI
TL;DR: Bone marrow‐derived mesenchymal stem cells (MSCs) hold great promise for treating immune disorders because of their immunoregulatory capacity, but the mechanism remains controversial, as it is shown here, the mechanism of MSC‐mediated immunosuppression varies among different species.
Abstract: Bone marrow-derived mesenchymal stem cells (MSCs) hold great promise for treating immune disorders because of their immunoregulatory capacity, but the mechanism remains controversial. As we show here, the mechanism of MSC-mediated immunosuppression varies among different species. Immunosuppression by human- or monkey-derived MSCs is mediated by indoleamine 2,3-dioxygenase (IDO), whereas mouse MSCs utilize nitric oxide, under the same culture conditions. When the expression of IDO and inducible nitric oxide synthase (iNOS) were examined in human and mouse MSCs after stimulation with their respective inflammatory cytokines, we found that human MSCs expressed extremely high levels of IDO, and very low levels of iNOS, whereas mouse MSCs expressed abundant iNOS and very little IDO. Immunosuppression by human MSCs was not intrinsic, but was induced by inflammatory cytokines and was chemokine-dependent, as it is in mouse. These findings provide critical information about the immunosuppression of MSCs and for better application of MSCs in treating immune disorders.

514 citations

Journal Article
TL;DR: Recent developments in the understanding of the antiviral and immunoregulatory properties of IFN-alpha, the nature of the multisubunit IFn-alpha receptor, and the molecular mechanisms of signal transduction are reviewed.
Abstract: IFNs were first described as potent antiviral agents 40 years ago, and recombinant IFN-alpha2a and IFN-alpha2b were approved for the treatment of hairy cell leukemia just 11 years ago Today, alpha-IFNs are approved worldwide for the treatment of a variety of malignancies and virologic diseases Although the exact mechanism of action of IFN-alpha in the treatment of such diseases is not fully understood, many advances have been made in the characterization of the physicochemical and diverse biological properties of this highly pleiotropic cytokine Here we review recent developments in our understanding of the antiviral and immunoregulatory properties of IFN-alpha, the nature of the multisubunit IFN-alpha receptor, and the molecular mechanisms of signal transduction Where available, we have included comparative data on recombinant alpha-IFNs derived from both naturally occurring and nonnaturally occurring synthetic genes We also review clinical data and data on the side effects and antigenicity of different sources of recombinant alpha-IFNs in humans These latter topics are of clinical interest, because they may potentially affect the efficacy of these various products Hopefully, what is already known about IFN will prompt further exploration into the mechanism(s) of action of IFN-alpha and thus deliver new applications for this prototypic cytokine, whose full therapeutic potential is yet to be realized

511 citations


Authors

Showing all 14639 results

NameH-indexPapersCitations
John Q. Trojanowski2261467213948
Virginia M.-Y. Lee194993148820
Danny Reinberg14534268201
Michael F. Holick145767107937
Tasuku Honjo14171288428
Arnold J. Levine139485116005
Aaron T. Beck139536170816
Charles J. Yeo13667276424
Jerry W. Shay13363974774
Chung S. Yang12856056265
Paul G. Falkowski12737864898
Csaba Szabó12395861791
William C. Roberts122111755285
Bryan R. Cullen12137150901
John R. Perfect11957352325
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20226
202113
20208
201917
201823
201736