Nat. Rev. Nephrol. doi: /nrneph

Slides:



Advertisements
Similar presentations
Lecture outline Types of hypersensitivity reactions
Advertisements

B-cell mediated disease
Figure 1 Schematic representation of idiopathic nephrotic syndrome,
“Systemic Lupus Erythematosus” (SLE): Pathophysiology
Volume 72, Issue 6, Pages (September 2007)
“Systemic Lupus Erythematosus” (SLE)
Systemic Lupus Erythematosus
Tumor Immunity: Exploring the Role of a Checkpoint
Figure 1 CTLA-4 and PD-1–PD-L1 immune checkpoints
Figure 2 Cell-mediated disease mechanisms of lupus nephritis
Figure 6 Effects of adiponectin on podocyte function
Figure 4 Interactions between adipose, the microbiome and kidney
Figure 1 Mechanisms of kidney injury in the setting of obesity
Volume 82, Issue 2, Pages (July 2012)
Figure 1 Pathological features of lupus nephritis subtypes
Figure 2 Systemic immune responses to cryptococcal antigen
Figure 2 Heat map of targeted therapies in autoimmune diseases
Figure 7 The efficacy of phosphate-binder therapy
Nat. Rev. Nephrol. doi: /nrneph
The Th17 immune response in renal inflammation
Figure 2 Expression of complement activation products in renal samples
Figure 1 Targets for monoclonal antibodies in B-cell lineages
Nat. Rev. Nephrol. doi: /nrneph
Figure 3 Nucleic acid sensors in SLE
Nat. Rev. Nephrol. doi: /nrneph
Figure 5 Comparison of outcomes with belimumab or rituximab therapy
Figure 3 TNFSF activities enhancing immune cell activation
Nat. Rev. Nephrol. doi: /nrneph
Figure 2 Co-stimulatory receptors as immunomodulatory targets
Figure 4 Combination immunotherapeutic approaches with imatinib
Figure 2 Molecular pathways involved in the regulation of T-cell differentiation and cytokine production Figure 2 | Molecular pathways involved in the.
Nat. Rev. Rheumatol. doi: /nrrheum
Figure 4 Macrophage-targeting antitumour treatment approaches
Nat. Rev. Urol. doi: /nrurol
Figure 2 Prevention of antigen–antibody
Figure 2 Roles of mTOR complexes in the kidney
Nat. Rev. Nephrol. doi: /nrneph
Figure 2 Altered innate immune functions after sepsis
Nat. Rev. Nephrol. doi: /nrneph
Nat. Rev. Nephrol. doi: /nrneph
Figure 4 The molecular configuration of the CD20 molecule
Nat. Rev. Nephrol. doi: /nrneph
Biological Therapies for Inflammatory Bowel Diseases
Nat. Rev. Nephrol. doi: /nrneph
B-Cell-Directed Therapy for Inflammatory Skin Diseases
Nat. Rev. Rheumatol. doi: /nrrheum
during the alloimmune response
Figure 2 Site of action of checkpoint inhibitors and agonists being
Complement in Kidney Disease: Core Curriculum 2015
Figure 3 Current model of immunopathogenesis in CIDP
Figure 3 Pathological activation of complement
Figure 3 Biologics that attenuate effector responses in the kidney
Nat. Rev. Rheumatol. doi: /nrrheum
Figure 1 The current model of the pathogenesis of SLE
Celiac Disease: From Pathogenesis to Novel Therapies
Nat. Rev. Nephrol. doi: /nrneph
Figure 2 Adaptive immunity in atherosclerosis
Nat. Rev. Rheumatol. doi: /nrrheum
Nat. Rev. Nephrol. doi: /nrneph
Figure 2 Biologics that target CD4+ T helper (TH)-cell subsets
Figure 1 Sequence of events in the development of autoimmune nephritis
Complement in Kidney Disease: Core Curriculum 2015
Figure 3 Preventive strategies for CSA-AKI
Figure 2 Cellular contributions to the development of SLE
Basophils and mast cells in renal injury
Understanding the pathogenesis of IgA nephropathy reveals therapeutic targets. Understanding the pathogenesis of IgA nephropathy reveals therapeutic targets.
EULAR Lupus Nephritis Trials Network Study Group
Novel therapies target the principal components of the immune system that contribute to LN pathogenesis. Novel therapies target the principal components.
Integrating intestinal microbiota into systemic lupus erythematosus (SLE) pathogenesis. Integrating intestinal microbiota into systemic lupus erythematosus.
(A–E) demonstrate a kidney biopsy from a patient with lupus nephritis (LN) class V. Representative micrographs: (A), an inflammatory infiltrate with T.
Presentation transcript:

Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.85 Figure 3 Therapeutic targets in systemic lupus erythematosus (SLE) and lupus nephritis Figure 3 | Therapeutic targets in systemic lupus erythematosus (SLE) and lupus nephritis. Greater understanding of the pathogenic processes underlying lupus nephritis has led to the identification of new therapeutic targets. B cells have a critical role in the pathogenesis of SLE, and B-cell depletion therapy therefore remains an attractive therapeutic option. The anti-CD20 antibody, rituximab, can deplete autoreactive B cells and thereby attenuate the production of autoantibodies involved in disease manifestations. The B-cell-activating factor (BAFF)-neutralizing antibody, belimumab, was shown to reduce renal flares and proteinuria in patients with SLE. Other promising B cell-depleting monoclonal antibodies, such as tabalumab and epratuzumab, require further testing. Abatacept is a co-stimulatory inhibitor that targets B7-1 (CD80) on the surface of dendritic cells or B cells, and blocks co-stimulation of CD28 on T cells. Inhibitors of the complement system, such as eculizumab and CCX-168 could have therapeutic value in patients with concurrent thrombotic microangiopathy or anti-neutrophil cytoplasmic antibody-associated vasculitis. Calcineurin inhibitors (CNIs) have immune modulatory effects but also direct effects on podocytes, and might be useful in patients with lupus-associated podocyte injury. Inhibition of the apoptosis regulator BCL-2 prevented the development of tubulointerstital inflammation in a mouse model of lupus nephritis. IL-23 activation might have a role in the development of glomerular crescents, suggesting that anti-IL-23 antibodies might be beneficial. Other promising therapies that need further exploration include infliximab, which targets the inflammatory tumour necrosis factor (TNF), sirukumab, which targets inflammatory IL-6, and monoclonal antibodies to interferon (IFN). GBM, glomerular basement membrane; TH17, T helper type 17 cell. Yu, F. et al. (2017) Redefining lupus nephritis: clinical implications of pathophysiologic subtypes Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.85