Institution
National Jewish Health
Healthcare•Denver, Colorado, United States•
About: National Jewish Health is a healthcare organization based out in Denver, Colorado, United States. It is known for research contribution in the topics: T cell & Asthma. The organization has 883 authors who have published 833 publications receiving 79201 citations. The organization is also known as: National Jewish Medical and Research Center.
Topics: T cell, Asthma, Population, Lung, Antigen
Papers published on a yearly basis
Papers
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22 Jan 2001TL;DR: In this article, the present invention relates to novel immortalized precursor cell populations derived from embryonic stem cell populations and methods to produce such cell populations, and an assay to identify regulatory compounds capable of controlling cell growth for therapeutic and experimental use.
Abstract: The present invention relates to novel immortalized precursor cell populations derived from embryonic stem cell populations and methods to produce such cell populations. Also disclosed is an assay to identify regulatory compounds capable of controlling cell growth for therapeutic and experimental use.
19 citations
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05 May 2000TL;DR: The amino acid and nucleic acid sequence of a protein expressed by monocytes and macrophages, called TALL-1, was disclosed in this paper, along with homologues, mimetics and antibodies that bind to it.
Abstract: The amino acid and nucleic acid sequence of a protein expressed by monocytes and macrophages, called TALL-1, are disclosed. Homologues, mimetics and antibodies that bind to TALL-1 are disclosed. Also disclosed is the TALL-1 receptor, and homologues of such receptor. The invention includes methods for regulating the interaction between TALL-1 and its receptor and for identifying compounds capable of such regulation. The invention also includes methods for regulating B lymphocyte proliferation, activation, and/or survival.
19 citations
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TL;DR: It is shown that peptide vaccines can expand T cells that naturally respond to tumor antigens, resulting in more effective antitumor immunity, and future immunotherapies may require similar stringent analysis of the responding T cells to select optimal peptides as vaccine candidates.
Abstract: A major goal of immunotherapy for cancer is the activation of T cell responses against tumor-associated antigens (TAAs). One important strategy for improving antitumor immunity is vaccination with peptide variants of TAAs. Understanding the mechanisms underlying the expansion of T cells that respond to the native tumor antigen is an important step in developing effective peptide-variant vaccines. Using an immunogenic mouse colon cancer model, we compare the binding properties and the TCR genes expressed by T cells elicited by peptide variants that elicit variable antitumor immunity directly ex vivo. The steady-state affinity of the natural tumor antigen for the T cells responding to effective peptide vaccines was higher relative to ineffective peptides, consistent with their improved function. Ex vivo analysis showed that T cells responding to the effective peptides expressed a CDR3β motif, which was also shared by T cells responding to the natural antigen and not those responding to the less effective peptide vaccines. Importantly, these data demonstrate that peptide vaccines can expand T cells that naturally respond to tumor antigens, resulting in more effective antitumor immunity. Future immunotherapies may require similar stringent analysis of the responding T cells to select optimal peptides as vaccine candidates.
19 citations
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TL;DR: It is hypothesized that germline-encoded components of the γδ TCRs provide for the specific recognition of a select set of antigenic determinants which appear on the cell surface in various molecular associations and serves to increase affinity for the molecules with which these Ags associate.
Abstract: After more than two decades of investigation, the biological role of the γδ T-cell receptors (TCRs) remains elusive. In fact, a theory of ligand recognition is still lacking that accounts for their adaptable structure, their peripheral selection, and the observed responses of γδ T cells, which do not require immunization but only include cells sharing germline-encoded components of the TCR. Assuming that all γδ T cells recognize ligands by a common mechanism, we now propose that germline-encoded components of the γδ TCRs provide for the specific recognition of a select set of antigenic determinants (Ags) which appear on the cell surface in various molecular associations. Furthermore, we hypothesize that the adaptivity of the γδ TCRs serves to increase affinity for the molecules with which these Ags associate rather than for the Ags themselves. Here we outline this hypothetical mechanism and discuss its possible implications for thymic selection and potential for complementing known innate and adaptive mechanisms of immune defense.
19 citations
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National Institutes of Health1, American College of Physicians2, Harvard University3, Georgetown University4, Icahn School of Medicine at Mount Sinai5, Henry Ford Health System6, Johns Hopkins University7, Medical University of South Carolina8, National Jewish Health9, University of Cincinnati10, University of Iowa11, University of Pennsylvania12
TL;DR: Simulation is conducted to compare the trend tests and the robust trend tests under various genetic models and the results are applied to detect candidate-gene association using an example from a case-control aetiologic study of sarcoidosis.
Abstract: Trend tests for genetic association using a matched case-control design are studied, which allows for a variable number of controls per case. However, the tests depend on the scores based on the underlying genetic model, thus it may result in substantial loss of power when the model is misspecified. Since the mode of inheritance may be unknown for complex diseases, robust trend tests in matched case-control studies are developed. Simulation is conducted to compare the trend tests and the robust trend tests under various genetic models. The results are applied to detect candidate-gene association using an example from a case-control aetiologic study of sarcoidosis.
18 citations
Authors
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Name | H-index | Papers | Citations |
---|---|---|---|
Thomas V. Colby | 126 | 501 | 60130 |
John W. Kappler | 122 | 464 | 57541 |
Donald Y.M. Leung | 121 | 614 | 50873 |
Philippa Marrack | 120 | 416 | 54345 |
Jeffrey M. Drazen | 117 | 693 | 52493 |
Peter M. Henson | 112 | 369 | 54246 |
David A. Schwartz | 110 | 958 | 53533 |
David A. Lynch | 108 | 714 | 59678 |
Norman R. Pace | 101 | 297 | 50252 |
Kevin K. Brown | 100 | 387 | 47219 |
Stanley J. Szefler | 99 | 554 | 37481 |
Erwin W. Gelfand | 99 | 675 | 36059 |
James D. Crapo | 98 | 473 | 37510 |
Yang Xin Fu | 97 | 390 | 33526 |
Stephen D. Miller | 94 | 433 | 30499 |