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Critical Reviews™ in Immunology

Publication de 6  numéros par an

ISSN Imprimer: 1040-8401

ISSN En ligne: 2162-6472

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.3 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.6 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00079 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.24 SJR: 0.429 SNIP: 0.287 CiteScore™:: 2.7 H-Index: 81

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T-Cell Receptor-Derived Peptides in Immunoregulation and Therapy of Retrovirally Induced Immunosuppression

Volume 21, Numéro 1-3, 2001, 18 pages
DOI: 10.1615/CritRevImmunol.v21.i1-3.40
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RÉSUMÉ

Retrovirally infected humans and mice showed progressive acquired immunodeficiency accompanied by the production of elevated levels of autoantibodies directed against T-cell receptor variable-domain epitopes. Epitope mapping analyses indicated that a major determinant recognized was defined by a 16-mer peptide containing the entire CDR1 segment and part of the FR2 region of human Vb8, and that both species showed reactivity to the same sequence. Either prophylactic or therapeutic administration of this peptide to retrovirusinfected C57/BL/6 mice normalized the balance of TH1- and TH2-type helper activity and restored the resistance to infection by the opportunistic parasite Cryptosporidium. Administration of the peptide did not generate significantly increased levels of autoantibody, but had a profound effect on T-cell activity as well as other aspects of inflammation, including NK-cell activity. A 16-mer derived from the Jb sequence showed similar functional effects on T cells from retrovirus-infected mice. Direct binding of the Vb CDR1 peptide to recombinant TCR Va/Vb constructs, as well as to IgM natural autoantibodies, suggests that the cell surface receptor for the peptide is the a/b TCR on T cells and surface IgM in B cells. The Vb CDR1 peptide stimulated division of murine splenocytes in vitro, stimulated the production of the TH1 cytokine IL-2, and synergized with the T-cell mitogen concanavalin A in proliferation and IL-2 production. These studies indicate that administration of peptides derived from T-cell receptor variable domains to animals immunosuppressed as a result of retroviral infection has a profound immunomodulatory effect enhancing overall T-cell functional capacity, particularly with respect to the cytokine production characteristic of TH1-type cells. Our studies are interpreted in the context of other recent investigations of immunomodulatory peptides.

CITÉ PAR
  1. Marchalonis John J., Jensen Ingvill, Schluter Samuel F., Structural, antigenic and evolutionary analyses of immunoglobulins and T cell receptors, Journal of Molecular Recognition, 15, 5, 2002. Crossref

  2. Sepúlveda Ramón Tomás, Marchalonis John Jacob, Watson Ronald Ross, T-Cell Receptor Vβ8.1 Peptide Reduces Coxsackievirus-induced Cardiopathology during Murine Acquired Immunodeficiency Syndrome, Journal of Cardiovascular Pharmacology, 41, 3, 2003. Crossref

  3. Marchalonis John J., Adelman Miranda K., Schluter Samuel F., Ramsland Paul A., The antibody repertoire in evolution: Chance, selection, and continuity, Developmental & Comparative Immunology, 30, 1-2, 2006. Crossref

  4. Yu Qianli, Watson Ronald R., Marchalonis John J., Larson Douglas F., A role for T lymphocytes in mediating cardiac diastolic function, American Journal of Physiology-Heart and Circulatory Physiology, 289, 2, 2005. Crossref

  5. Yu Qianli, Vazquez Randy, Zabadi Sherma, Watson Ronald R., Larson Douglas F., T-lymphocytes mediate left ventricular fibrillar collagen cross-linking and diastolic dysfunction in mice, Matrix Biology, 29, 6, 2010. Crossref

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