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Critical Reviews™ in Immunology

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ISSN Печать: 1040-8401

ISSN Онлайн: 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 Basis of Immunogenicity of Endocrine Allografts

Том 21, Выпуск 1-3, 2001, 15 pages
DOI: 10.1615/CritRevImmunol.v21.i1-3.60
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Краткое описание

Two signals are required for optimal T-cell activation: the engagement of the antigen-specific receptor and the provision of a second non–antigen-specific inductive signal, or costimulator (CoS). Regarding allograft immunity, two primary pathways of donor antigen presentation can fulfill this two-signal requirement, resulting in cellular immunity to a transplant: (1) "direct" (donor MHC-restricted) presentation in which the antigen-presenting cells (APCs) resident within the transplant directly activate host T lymphocytes and (2) "indirect" (host MHC-restricted) presentation in which host-derived APCs acquire donor antigens that are then presented to host T lymphocytes. It appears that endocrine allografts, such as pancreatic islets and thyroid, are highly dependent on donor-derived APCs, or "passenger leukocytes," to trigger acute graft rejection. Tissue pretreatment aimed at selectively eliminating APCs within endocrine tissues can result in indefinite allograft survival in immune-competent recipients. Although such results implicate the “direct” pathway as the predominant route of host sensitization, the role of donor APCs in rejection appears to be more complex. Recently, we have found that indirect, CD4 T-cell–dependent reactivity can contribute to islet allograft rejection. However, such indirect recognition nevertheless requires donor-derived APCs as a source of antigen. Thus, whereas the donor-type APC is a critical limiting step for initiating islet allograft rejection, such cells can trigger both direct and indirect forms of immune responses that can result in graft rejection. That is, donor hematopoietic cells, rather than tissue parenchymal cells, probably play a major role in providing antigens that stimulate cellular immunity.

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