Distributed Denial-of-Service (DDoS) attacks have become a critical threat to the Internet. Due to the increasing number of vulnerable Internet of Things (IoT) devices, attackers can easily compromise a large set of nodes and launch highvolume DDoS attacks from the botnets. State-of-the-art DDoS defenses, however, have not caught up with the fast development of the attacks. Middlebox-based defenses can achieve high performance with specialized hardware; however, these defenses incur a high cost, and deploying new defenses typically requires a device upgrade. On the other hand, software-based defenses are highly flexible, but software-based packet processing leads to high performance overheads. In this paper, we propose POSEIDON, a system that addresses these limitations in today's DDoS defenses. It leverages emerging programmable switches, which can be reconfigured in the field without additional hardware upgrade. Users of POSEIDON can specify their defense strategies in a modular fashion in the form of a set of defense primitives; this can be further customized easily for each network and extended to include new defenses. POSEIDON then maps the defense primitives to run on programmable switches-and when necessary, on server software-for effective defense. When attacks change, POSEIDON can reconfigure the underlying defense primitives to respond to the new attack patterns. Evaluations using our prototype demonstrate that POSEIDON can effectively defend against highvolume attacks, easily support customization of defense strategies, and adapt to dynamic attacks with low overheads.

Behçet’s disease (BD) is a chronic vasculitis characterized by systemic immune aberrations. However, a comprehensive understanding of immune disturbances in BD and how they contribute to BD pathogenesis is lacking. Here, we performed single-cell and bulk RNA sequencing to profile peripheral blood mononuclear cells (PBMCs) and isolated monocytes from BD patients and healthy donors. We observed prominent expansion and transcriptional changes in monocytes in PBMCs from BD patients. Deciphering the monocyte heterogeneity revealed the accumulation of C1q-high (C1q hi ) monocytes in BD. Pseudotime inference indicated that BD monocytes markedly shifted their differentiation toward inflammation-accompanied and C1q hi monocyte–ended trajectory. Further experiments showed that C1q hi monocytes enhanced phagocytosis and proinflammatory cytokine secretion, and multiplatform analyses revealed the significant clinical relevance of this subtype. Mechanistically, C1q hi monocytes were induced by activated interferon-γ (IFN-γ) signaling in BD patients and were decreased by tofacitinib treatment. Our study illustrates the BD immune landscape and the unrecognized contribution of C1q hi monocytes to BD hyperinflammation, showing their potential as therapeutic targets and clinical assessment indexes.