期刊
CRITICAL REVIEWS IN IMMUNOLOGY
卷 29, 期 1, 页码 69-86出版社
BEGELL HOUSE INC
DOI: 10.1615/CritRevImmunol.v29.i1.30
关键词
cell death; alarmins; cross-presentation; dendritic cells; autoimmunity; tissue repair
类别
资金
- Italian Association for Cancer Research
- Association for International Cancer Research
- Ministry of University and Research
- Ministry of Health
- Fondazione Cariplo
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, Th17, 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-mediated protective immunity, tissue repair, persistent inflammation and autoimmunity, or tolerance.
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