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Critical Reviews™ in Immunology

Publicou 6 edições por ano

ISSN Imprimir: 1040-8401

ISSN On-line: 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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Expression of T Lymphocyte Adhesion Molecules: Regulation During Antigen-Induced T Cell Activation and Differentiation

Volume 18, Edição 3, 1998, pp. 153-184
DOI: 10.1615/CritRevImmunol.v18.i3.10
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RESUMO

The pattern of lymphocyte traffic and migration in vivo is a composite of constitutive recirculation and transient changes induced by interaction with antigen. Naive T lymphocytes in their basal, unstimulated state continuously recirculate throughout the entire host, poised to react to specific antigens that they are programmed to recognize. After interaction with antigen, T cell traffic changes, first with the trapping of reactive cells in antigen-containing lymphoid tissue. Subsequently, the effector cells responding to antigen, accompanied by nonspecific T cells and monocytes, traffic in large numbers to sites of antigen localization, resulting in the localized inflammatory response. Then, as the immune response wanes, memory T cells develop, many of which exhibit still different routes of recirculation. The traffic and tissue localization of leukocytes is regulated by a series of cell surface adhesion molecules that recognize specific ligands on endothelial cells and in the extracellular matrix. Modulation of the expression of these adhesion molecules results in the changes in T cell traffic that are characteristic of each stage of T cell differentiation. Thus, during T cell activation and differentiation, the down-regulation of adhesion receptors specific for lymphoid tissue endothelium and up-regulation of integrins facilitate the targeting of effector cells to sites of inflammation. Subsequent changes in adhesion receptors regulate the traffic of the antigen-specific memory cells. T cell adhesion molecule expression is therefore regulated as a function of the stage of activation and differentiation and, in addition, is influenced by cytokines and the local lymphoid microenvironment.

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