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Human beings are constantly exposed to pathogens. The innate immune system is the first line of defense against microbes. It has evolved to recognize conserved microbial motifs (PAMP or pathogen-associated molecular patterns) thanks to a limited array of receptors termed pattern recognition receptors (PRR). Upon activation, most PRR trigger a transcriptional response leading to neosynthesis of hundreds of genes. In contrast, engagement of various PRR in the recently identified inflammasome complexes lead to activation of a cysteine protease, caspase-1. This inflammatory caspase has a dual activity: it triggers the release of very potent proinflammatory cytokines IL-1β and IL-18 and, an hyperinflammatory cell death termed pyroptosis. In this review, we describe the inflammasome receptors and their ligands, the molecular mechanisms leading to the assembly of this innate immune platform and the role of the inflammasome during viral and bacterial infections., (© 2013 médecine/sciences – Inserm.)

Giant cell arteritis is a large-vessel vasculitis affecting all three layers of the arterial wall. Histopathology of this vasculitis consists of an inflammatory infiltrate with CD4(+) T cells, macrophages, multinucleated giant cells, forming granulomas in the media. This infiltrate is associated with a destruction of the arterial wall, a fragmentation of the internal elastic lamina and a vascular remodeling leading to intimal hyperplasia. Recent studies have clarified the role of Th17 cells in the initial phase of the disease, pro-inflammatory cytokines and vascular smooth muscle cells in vascular remodeling. This review aims to update data on giant cell arteritis pathogenesis and to propose clues of investigation for a better understanding of this condition., (Copyright © 2013 Société nationale française de médecine interne (SNFMI). Published by Elsevier SAS. All rights reserved.)