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Critical Reviews™ in Immunology

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ISSN Druckformat: 1040-8401

ISSN Online: 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

IgM-Mediated B Cell Apoptosis

Volumen 15, Ausgabe 3-4, 1995, pp. 255-269
DOI: 10.1615/CritRevImmunol.v15.i3-4.40
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ABSTRAKT

Cross-linking of surface immunoglobulin M (slgM) on normal mature B cells induces different signaling consequences, including DNA synthesis (positive signaling) and cell cycle arrest and/or death by apoptosis (negative signaling). Presumably, the difference depends on the intensity of slgM cross-linking: relatively weak cross-linking induces DNA synthesis, moderate cross-linking induces DNA synthesis with cell cycle arrest at the G2/M interphase, and intense cross-linking induces apoptosis. In vivo experiments with transgenic mice have shown that relatively weak cross-linking of slgM by soluble antigens induces anergy in autoreactive B cells, whereas intense slgM cross-linking by membrane-bound forms of antigens induces deletion of them. However, it is still unknown whether the different intensities of slgM cross-linking generate qualitatively different signals responsible for DNA synthesis or cell death or whether they generate qualitatively the same but quantitatively different signals, and the quantitative difference is responsible for the induction of positive or negative signaling. The slgM-mediated negative signaling presumably plays an important role in the induction and maintenance of B cell tolerance, and slgD and slgG also possess the machinery necessary for negative signaling. Negative signaling through slgM is dependent on tyrosine kinase(s) and Ca2+ influx and is sensitive to cyclosporin A in certain types of B cells but not in all B cells. It has been suggested that there are different intracellular signaling pathways that transduce negative signaling via slgM, and that activation-induced B cell death by slgM cross-linking does not necessarily show DNA fragmentation and the morphology of apoptosis. On the other hand, slgM-mediated B cell death may be inhibited in the presence of appropriate co-stimulators such as IL-4, α-, and β-interferons and CD40-mediated signaling. The CD40-mediated signaling effectively inhibits slgM-mediated B cell apoptosis in many but not all experimental systems. Although homotypic cell adhesion through the LFA-1/ICAM-1 dependent pathway was shown to be involved in certain types of CD40-mediated inhibition of slgM-mediated negative signaling, it is still not known how the cytokines and CD40-mediated signaling inhibit slgM-mediated B cell death. The molecular mechanisms responsible for slgM-mediated negative signaling and for the inhibitory signaling against slgM-mediated negative signaling need further elucidation.

SCHLÜSSELWÖRTER: IgM, B cell, Apoptosis, CD40, LFA-l/ICAM-1
REFERENZIERT VON
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