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Critical Reviews™ in Immunology

Publicado 6 números por año

ISSN Imprimir: 1040-8401

ISSN En Línea: 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

Indexed in

Regulation of Regulatory T Cells: Role of Dendritic Cells and Toll-Like Receptors

Volumen 26, Edición 4, 2006, pp. 291-306
DOI: 10.1615/CritRevImmunol.v26.i4.10
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SINOPSIS

Regulatory T cells (Treg) are characterized by high-level surface CD25 and intracellular FoxP3 expression. Treg are instrumental in the maintenance of peripheral immune tolerance and the control of adaptive immune responses. Naturally occuring Treg suppress T-cell responses by cell contact-dependent mechanisms, whereas induced regulatory cells, including Tr1 cells, secrete inhibitory cytokines such as transforming growth factor (TGF)-β and interleukin-10. The interplay between Treg and antigen-responsive T cells is modulated by dendritic cells (DC). Whereas immature myeloid precursors of DC suppress T-cell activation per se and immature DC support Treg development, mature DC can override Treg-mediated suppression in vitro and in vivo. Mature DC activated through Toll-like receptor (TLR) pattern recognition receptors produce proinflammatory cytokines, including interleukin-6, which render responder T cells refractory to the suppressive effect of Treg. In addition, Treg also express certain TLR, and the activation and/or suppressor function of Treg is modulated directly by the respective ligands. In this review, we discuss current models of how signals delivered through innate immune receptors in response to pathogen-associated molecular patterns affect adaptive immune responses via modulation of Treg function.

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