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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Critical Reviews™ in Immunology
Импакт фактор: 1.352 5-летний Импакт фактор: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Печать: 1040-8401
ISSN Онлайн: 2162-6472

Выпуски:
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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v29.i1.30
pages 69-86

Regulation of Dendritic- and T-Cell Fate by Injury-Associated Endogenous Signals

Angelo A. Manfredi
Vita-Salute San Raffaele University & San Raffaele Scientific Institute, 20132 Milano, Italy
Annalisa Capobianco
Vita-Salute San Raffaele University & San Raffaele Scientific Institute, 20132 Milano, Italy
Marco E. Bianchi
Vita-Salute San Raffaele University & San Raffaele Scientific Institute, 20132 Milano, Italy
Patrizia Rovere-Querini
Vita-Salute San Raffaele University & San Raffaele Scientific Institute, 20132 Milano, Italy

Краткое описание

Two events characterize tissue injury and sterile inflammation: (1) generation/release of autoantigens, and (2) generation of homeostatic inflammatory signals. Homeostatic signals recruit leukocytes and promote cell migration and division to replace injured cells. Moreover, they activate antigen-presenting phagocytes, in particular, dendritic cells (DCs), in anticipation of microbial invasion. Activated DCs undergo a differentiation process, referred to as maturation, and migrate to secondary lymphoid organs. Maturing DCs upregulate the molecular machinery required for the priming of naive T cells, including T lymphocytes recognizing autoantigens, which represent a substantial fraction of the host T-cell repertoire. Recent data indicate that cues generated at sites of injury shape T-cell clonal expansion, regulating sensitivity to activation-dependent apoptosis and commitment towards a Th1, Th2, Th7, or regulatory T-cell fate. Endogenous signals of tissue injury, also called damage-associated molecular patterns (DAMPS) or alarmins, therefore provide a code for switching the outcome of the presentation of autoantigens towards results as diverse as T-cell-mcdiated protective immunity, tissue repair, persistent inflammation and autoimmunity, or tolerance.