Nat. Rev. Rheumatol. doi: /nrrheum

Slides:

Advertisements

Similar presentations

Nat. Rev. Rheumatol. doi: /nrrheum

Advertisements

Figure 3 The adaptive and maladaptive energy matrices

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 3 Metabolism in homeostatic chondrocytes

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Induction of immune tolerance

Figure 4 Simplified T cell and antigen presenting

Figure 5 Defects in the JAK–STAT signalling pathway

Figure 2 Main functions of IL-1

NOD-like and Toll-like receptors or inflammasomes contribute to kidney disease in a canonical and a non-canonical manner Hans-Joachim Anders, Maciej.

Figure 1 Metabolic profiling as a tool for studying rheumatic diseases

Figure 1 Immune mechanisms in liver homeostasis

Schematic summary of innate signaling pathway components and filaments

Figure 7 Defects in apoptosis

Figure 3 Nucleic acid sensors in SLE

Figure 3 TNFSF activities enhancing immune cell activation

Toll-like receptor activation: from renal inflammation to fibrosis

Figure 3 Defects in the T cell receptor signalling pathway

Figure 3 Molecular mechanisms of crystal-induced necroinflammation

Microbial Symbiosis with the Innate Immune Defense System of the Skin

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Neurol. doi: /nrneurol

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 3 Strategies to achieve therapeutic inhibition of IL-1

Figure 4 Macrophage-targeting antitumour treatment approaches

Nat. Rev. Urol. doi: /nrurol

Figure 1 Activation and signalling of IL-1

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 3 Statistical approaches for the analysis of metabolomic data

Nat. Rev. Rheumatol. doi: /nrrheum

Dieter Demon, Lieselotte Vande Walle, Mohamed Lamkanfi

Figure 5 The role of Ly6Chi and Ly6Clo monocytes

Figure 4 Macrophages in liver inflammation

Figure 3 Effect of sialylated glycoforms on IgG activity

Figure 3 Multi-hit model for autoimmune diseases

To the heart of the APS puzzle

and obesity-related kidney diseases

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 4 Role of TGFβ in a normal and an osteoarthritic joint

Figure 4 TNFSF inflammatory activities in tissue cells

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 3 Inflammatory mechanisms in tendinopathy

Chadrick E. Denlinger, MD

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Transmission of pain by NGF

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 2 Biologics that target CD4+ T helper (TH)-cell subsets

Figure 2 A model of TNFR–complex I signalling

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Chronic inflammation and DNA damage in people with SLE

Figure 3 Nuclear-penetrating autoantibodies and synthetic lethality

Figure 1 Extrinsic and intrinsic pathways of apoptosis

Figure 1 The role of macrophages in RA

Figure 2 The main effects of adipokines on bone remodelling in osteoarthritis Figure 2 | The main effects of adipokines on bone remodelling in osteoarthritis.

Figure 2 Glatiramer acetate treatment induced M2 differentiation through a MyD88-independent pathway (A) As described previously,3 M2 monocytes were treated.

Primary immunodeficiencies may reveal potential infectious diseases associated with immune-targeting mAb treatments László Maródi, MD, PhD, Jean-Laurent.

Hypothesized mechanisms of air pollution–mediated cardiometabolic disease wherein inhalational or nutritional signals either directly or via the generation.

Macrophages, Immunity, and Metabolic Disease

Figure 5 TLR-dependent signaling pathways inhibited by glatiramer acetate Myeloid differentiation primary response gene 88 (MyD88) and Toll-IL-1 receptor.

CD14: Chaperone or Matchmaker?

Predicted sequence of events in O. volvulus/Wolbachia-induced keratitis. Predicted sequence of events in O. volvulus/Wolbachia-induced keratitis. Wolbachia.

Toll-like receptors, adapter proteins, and signaling molecules.

Presentation transcript:

Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2016.132 Figure 3 Caspase 8 is required for normal M1 macrophage polarization in vitro Figure 3 | Caspase 8 is required for normal M1 macrophage polarization in vitro. a | Following treatment with IFNγ and lipopolysaccharide (LPS) to induce M1 macrophage polarization in vitro, caspase 8 can block receptor interacting serine/threonine protein kinase 1 (RIPK1) signalling. b | In the absence of caspase 8, RIPK1 signalling proceeds unchecked, leading to an abnormal response in M1 macrophage polarization. c | Blockade of RIPK1 signalling, via chemical inhibition with necrostatin 1 (NEC1), restores normal M1 polarization of caspase 8-deficient macrophages. MYD88, myeloid differentiation primary response protein MYD88; TRIF, TIR domain-containing adapter protein inducing interferon-beta, also known as TICAM1. Cuda, C. M. et al. (2016) The inflammatory role of phagocyte apoptotic pathways in rheumatic diseases Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2016.132