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Critical Reviews™ in Immunology

Published 6 issues per year

ISSN Print: 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

The Granule Pathway of Programmed Cell Death

Volume 25, Issue 3, 2005, pp. 161-182
DOI: 10.1615/CritRevImmunol.v25.i3.10
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ABSTRACT

The exocytosis of death-inducing granzymes stored in the granules of cytotoxic lymphocytes allows the immune system to rapidly eliminate intracellular pathogens and transformed cells. The membrane-disrupting protein perforin allows the entry of granzymes into a cell, where they induce apoptosis by cleaving target substrates in the cytoplasm and nucleus. Granzymes kill cells in a variety of ways. Recent work has demonstrated that granzymes induce mitochondrial dysfunction through caspase and caspase-independent pathways and destroy DNA and the integrity of the nucleus. Cytotoxic lymphocytes are susceptible to self-inflicted damage. Mice and humans defective in perforin and granzymes point to a role for self-inflicted damage in downregulating lymphocyte responses. Given the propensity for the granule pathway to inflict cellular damage, cytotoxic lymphocytes have developed a variety of mechanisms to protect themselves. In this regard, endogenous serine protease inhibitors have been suggested to protect cytotoxic lymphocytes from granzyme B. It would appear that certain viruses and possibly even tumor cells also use the same mechanism to escape destruction from the exocytosis pathway of programmed cell death.

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  3. Khurshid Rukhshan, Saleem Mahjabeen, Akhtar Muhammad Saleem, Salim Asmat, Granzyme M: characterization with sites of post-translational modification and specific sites of interaction with substrates and inhibitors, Molecular Biology Reports, 38, 5, 2011. Crossref

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  5. Howe Charles L., Adelson Jaimie D., Rodriguez Moses, Absence of perforin expression confers axonal protection despite demyelination, Neurobiology of Disease, 25, 2, 2007. Crossref

  6. Strik Merel C.M., de Koning Pieter J.A., Kleijmeer Monique J., Bladergroen Bellinda A., Wolbink Angela M., Griffith Janice M., Wouters Dorine, Fukuoka Yoshihiro, Schwartz Lawrence B., Hack C. Erik, van Ham S. Marieke, Kummer J. Alain, Human mast cells produce and release the cytotoxic lymphocyte associated protease granzyme B upon activation, Molecular Immunology, 44, 14, 2007. Crossref

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