Figure 2 Cellular contributions to the development of SLE

Slides:

Advertisements

Similar presentations

Pathogenesis of systemic lupus erythematosus (SLE)

Advertisements

Volume 72, Issue 6, Pages (September 2007)

The beauty of TLR agonists for CTCL

Figure 1 CTLA-4 and PD-1–PD-L1 immune checkpoints

Figure 2 Cell-mediated disease mechanisms of lupus nephritis

Nat. Rev. Nephrol. doi: /nrneph

Figure 5 Involvement of B cells in SLE

Figure 3 Neutrophils in liver inflammation

Figure 1 Radiation-induced effects on tumour cells

Figure 5 Dendritic cells in liver inflammation

Figure 1 Induction of immune tolerance

Figure 3 Proposed mechanisms underlying the links

Figure 2 Heat map of targeted therapies in autoimmune diseases

Figure 2 Main functions of IL-1

Figure 4 Involvement of SEMA4D in the pathogenesis

Nat. Rev. Nephrol. doi: /nrneph

Adaptive Immune System

Figure 1 Targets for monoclonal antibodies in B-cell lineages

Figure 4 Antinuclear antibodies and disease activity in SLE

Figure 3 Transcriptome studies performed in the target

Figure 3 Nucleic acid sensors in SLE

Neutrophils, dendritic cells and macrophages deliver activation signals to marginal zone B cells. Neutrophils, dendritic cells and macrophages deliver.

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 Location of HLA variants known to be associated

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 TNFSF activities enhancing immune cell activation

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Cardiol. doi: /nrcardio

Figure 1 Intrathymic T-cell differentiation

Nat. Rev. Rheumatol. doi: /nrrheum

Minyoung Her, MD, Arthur Kavanaugh, MD

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 2 Emerging models of antibody-mediated rejection (ABMR) and

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Rheumatol. doi: /nrrheum

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 4 TNFSF inflammatory activities in tissue cells

Figure 3 Current model of immunopathogenesis in CIDP

Figure 2 Pro-inflammatory and anti-inflammatory effects of the gut microbiota Figure 2 | Pro-inflammatory and anti-inflammatory effects of the gut microbiota.

Figure 3 Biologics that attenuate effector responses in the kidney

Autoimmunity through Cytokine-Induced Dendritic Cell Activation

Figure 1 Treat to target, remission and low disease activity in SLE

Figure 1 The current model of the pathogenesis of SLE

Nat. Rev. Nephrol. doi: /nrneph

Figure 2 GM-CSF — a key player in inflammation and autoimmunity

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 1 NETosis pathways and potential therapeutic targets

Role of IgE in autoimmunity

Figure 1 The release of DNA from dead and dying cells

Figure 1 Sequence of events in the development of autoimmune nephritis

Adiponectin: an enlarging role in acute kidney injury

Figure 1 Chronic inflammation and DNA damage in people with SLE

Figure 3 Nuclear-penetrating autoantibodies and synthetic lethality

Deficiency of TLR9 promotes more severe renal inflammation in imiquimod-induced autoimmunity. Deficiency of TLR9 promotes more severe renal inflammation.

Figure 2 Initiators of obesity-associated inflammation in adipocytes

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 3 Underlying mechanisms of TREG cells in atherosclerosis

Figure 4 Role of chemokines in dendritic cell migration

Figure 1 The role of macrophages in RA

SLE: the many players involved in systemic autoimmunity and tissue destruction. SLE: the many players involved in systemic autoimmunity and tissue destruction.

IFNα Induces MDSC Maturation and Loss of Suppressive Function

Nat. Rev. Rheumatol. doi: /nrrheum

A schematic presentation of secreted, endocytic, and signaling pattern-recognition receptors. A schematic presentation of secreted, endocytic, and signaling.

Jacques Banchereau, Virginia Pascual Immunity

Integrating intestinal microbiota into systemic lupus erythematosus (SLE) pathogenesis. Integrating intestinal microbiota into systemic lupus erythematosus.

Cytokines and cytokine receptors involved in type I immunity in tuberculosis. Cytokines and cytokine receptors involved in type I immunity in tuberculosis.

Figure 2 Involvement of plasmacytoid dendritic cells

Presentation transcript:

Figure 2 Cellular contributions to the development of SLE Figure 2 | Cellular contributions to the development of SLE. Neutrophils and apoptotic cells are at the apex of the cascade of pathogenetic mechanisms in systemic lupus erythematosus (SLE). They provide the critical ligands to drive expression of type I interferons (IFNs). Neutrophils represent a key inflammatory participant in organ damage; these cells also release neutrophil extracellular traps (NETs), a source of citrullinated peptide and nucleic acid antigens, via NETosis. Many cells produce type I IFNs, but plasmacytoid dendritic cells produce the highest levels of these cytokines. Apoptotic debris can also activate inflammatory cytokine expression which participates in the recruitment of cells into tissues. T cells and B cells both participate in autoreactivity, with B cells ultimately producing autoantibodies. T-cell production of IL-17 also contributes to organ infiltration by neutrophils. BAFF, B-cell activating factor; BAFF-R, BAFF receptor; CAMP, cathelicidin antimicrobial peptide; FcR, Fc receptor; MHC, major histocompatibility complex; TACI, transmembrane activator and cyclophilin ligand interactor; TLR, Toll-like receptor. Tsokos, G. C. et al. (2016) New insights into the immunopathogenesis of systemic lupus erythematosus Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2016.186