(A–E) demonstrate a kidney biopsy from a patient with lupus nephritis (LN) class V. Representative micrographs: (A), an inflammatory infiltrate with T.

Slides:

Advertisements

Similar presentations

Volume 72, Issue 7, Pages (October 2007)

Advertisements

Volume 68, Issue 4, Pages (October 2005)

Volume 79, Issue 11, Pages (June 2011)

Anifrolumab inhibits cytokine production, plasmacytoid dendritic cell (pDC) activation and the type I (interferon gene signature) IFN gene signature. Anifrolumab.

Figure 1 Pathological features of lupus nephritis subtypes

Osteopontin expression in human crescentic glomerulonephritis

Histomorphology in a case of mixed (cellular and humoral) acute kidney allograft rejection (patient 10). Histomorphology in a case of mixed (cellular and.

Volume 68, Issue 6, Pages (December 2005)

Anifrolumab inhibits type I interferon (IFN)-induced IFN-stimulated response element (ISRE) signalling. Anifrolumab inhibits type I interferon (IFN)-induced.

Time between systemic lupus erythematosus (SLE) and haematological malignancy diagnoses. Time between systemic lupus erythematosus (SLE) and haematological.

Quiz Page February 2016 American Journal of Kidney Diseases

Immunohistochemistry of CD8 (A and B) and PD-L1 (C–F).

Volume 74, Issue 4, Pages (August 2008)

Volume 74, Issue 1, Pages (July 2008)

Sven Y. Surikow et al. BTS 2018;3:

Fig. 1 pDCs infiltrate the skin of SSc patients and spontaneously secrete IFN-α and CXCL4. pDCs infiltrate the skin of SSc patients and spontaneously secrete.

Correlation between disease activity and phospho-H2AX levels at G0/G1, S and G2 cell-cycle phases in primary CD3+ T cells and monocytes from patients with.

Fig. 4 Expression of cleaved caspase 3, PD-L1, and PD-1 in HGGs after reovirus treatment. Expression of cleaved caspase 3, PD-L1, and PD-1 in HGGs after.

Volume 68, Issue 4, Pages (October 2005)

Volume 75, Issue 12, Pages (June 2009)

Lupus Nephritis: Mesangial and Membranous Forms (WHO II and V)

Volume 68, Issue 6, Pages (December 2005)

Immunohistochemistry staining of interferon (IFN)-λ in renal tissue.

Lupus Nephritis: Proliferative Forms (WHO III, IV)

Association of AIM2, RIG‐I and NLRP3 inflammasomes with better survival in NPC patients.A.Overexpression of ASC, caspase‐1 and IL‐1β proteins as well as.

Volume 70, Issue 2, Pages (July 2006)

Volume 95, Issue 3, Pages (March 2019)

TLR9 deficiency promotes aberrant T cell and myeloid dendritic cell (DC) phenotype in imiquimod-induced autoimmunity. TLR9 deficiency promotes aberrant.

Volume 62, Issue 2, Pages (August 2002)

Volume 72, Issue 7, Pages (October 2007)

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

Virus-specific T cell responses are detected in all MERS survivors.

Histological and mRNA analysis of the inflammatory cytokines in the vehicle‐ or etifoxine‐treated mice at onset of clinical symptoms.A–D.At day 10 p.i.,

Serum osteopontin (OPN) levels in population-based controls and in cases with SLE. Serum levels of OPN, determined by ELISA, were significantly higher.

Immunohistochemistry (IHC) staining of interferon (IFN)-λ in renal tissue The figure demonstrates a repeated renal biopsy obtained from a patient after.

Class IV-S versus class IV-G lupus nephritis: Clinical and morphologic differences suggesting different pathogenesis Gary S. Hill, Michel Delahousse,

Volume 69, Issue 10, Pages (May 2006)

No difference in T-cell response between SLE patients and healthy controls upon superantigen stimulation. No difference in T-cell response between SLE.

Receiver operating curve of soluble C3, C4, antibodies to double-stranded DNA (anti-dsDNA) compared with complement C4d levels on erythrocytes (EC4d) and.

Longitudinal changes in serum G3BP concentrations and SLEDAI in 15 patients with SLE. Each plot represents one patient. Longitudinal changes in serum G3BP.

Significant pathological changes and activation of Nrf2 pathway in the glomeruli of human diabetic nephropathy patients. Significant pathological changes.

Anifrolumab does not elicit antibody-dependent cell-mediated cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC) activity. Anifrolumab does.

Fig. 1 Intrarenal lymphangiogenesis in patients with CKD accompanied by intrarenal inflammatory cells and renal fibrosis. Intrarenal lymphangiogenesis.

Correlation between mean Safety of Estrogens in Lupus Erythematosus National Assessment–Systemic Lupus Erythematosus Disease Activity Index (SELENA-SLEDAI)

Anti-RNP/anti-Sm antibodies in sera (bleeds 1–5) and H&E stained sections of kidney/salivary gland of the MRL-lpr/lpr and MRL-MpJ mice provided with water,

Silver-stained gel showing the major tyrosine-phosphorylated proteins in podocytes. Silver-stained gel showing the major tyrosine-phosphorylated proteins.

Correlations between two measures of type I interferon activity and serum galectin-3-binding protein in the SLE-IFN-α (n=26) and HC-IFN-α (n=10) cohorts.

The effect of purified IgG from healthy controls or patients with lupus nephritis on tyrosine phosphorylation in podocytes at two different IgG concentrations.

Insulitis is reduced in CT-treated RIP-LCMV-GP mice.

Tyrosine phosphorylation of proteins in podocyte lysates following exposure to healthy or lupus nephritis plasma. Tyrosine phosphorylation of proteins.

Comparison of the effects of growing podocytes in plasma from patients with lupus nephritis (LN), rheumatoid arthritis or non-renal lupus. Comparison of.

Hierarchical clustering of non-classical monocytes from patients and controls, with tracks indicating individuals, IFN score, SLEDAI score and prednisone.

Representative example of gating on T-cell subpopulations.

SLE deconvolution patient clusters and representative immune cell types (A), and distribution of patients by SLE deconvolution cluster and treatment group—all.

Antibody levels to Ro52, Ro60, p200 and La antigens in control and congenital heart block (CHB) cohort were measured as bound units (BU). Antibody levels.

Immune cell populations associated with type I IFNGS test status and disease activity. Immune cell populations associated with type I IFNGS test status.

Serum anti-neuronal antibodies (anti-N) in patients with positive serum anti-GRP78. Serum anti-neuronal antibodies (anti-N) in patients with positive serum.

Geographic colocalization of PD-L1+ tumor cells with infiltrating immune cells in MCC. The predominant pattern of tumor cell PD-L1 expression is at the.

Overall gene expression in monocyte subsets in patients and controls.

(A) Mean urine protein/creatinine ratio (UPCR) and SEM in participants from the combined Lupus Nephritis Assessment of Rituximab (LUNAR) and A Study to.

IFN-γ-producing T-cells in SLE patients and healthy controls upon EBV antigen stimulation. IFN-γ-producing T-cells in SLE patients and healthy controls.

Activated T-cells in SLE patients and healthy controls upon EBV antigen stimulation. Activated T-cells in SLE patients and healthy controls upon EBV antigen.

Bronchial biopsy from patient 5 (a; Haematoxylin-Eosin-Safran stain and ×10 growth). Bronchial biopsy from patient 5 (a; Haematoxylin-Eosin-Safran stain.

PD-L1 is expressed in breast cancer.

Median percentage change in complement components 3 and 4 over time by SLE deconvolution cluster—all randomised and treated patients.* *Data from five.

TLR9 deficiency leads to more severe impairment of endothelium-dependent vasorelaxation and promotes aberrant B cell phenotype in imiquimod-induced autoimmunity.

Fig. 7 BEL immune response.

Overall and recurrence-free survival.

CD36 expression is coordinately regulated in multiple cellular compartments. CD36 expression is coordinately regulated in multiple cellular compartments.

CD36 expression in tissue adjacent and distal to the tumor.

Presentation transcript:

(A–E) demonstrate a kidney biopsy from a patient with lupus nephritis (LN) class V. Representative micrographs: (A), an inflammatory infiltrate with T cells as demonstrated by a positive CD3 staining. (A–E) demonstrate a kidney biopsy from a patient with lupus nephritis (LN) class V. Representative micrographs: (A), an inflammatory infiltrate with T cells as demonstrated by a positive CD3 staining. (B), demonstration of interferon (IFN)-λ staining, predominantly found in the inflammatory infiltrate shown in (A) but also present in the glomeruli. (C), the same infiltrate from a consecutive section, stained with irrelevant isotype control antibody. (D), another part of the biopsy from the same patient, showing an inflammatory infiltrate with T cells as demonstrated by positive CD3 staining. (E), demonstration of IFNλ staining in that infiltrate. Original magnifications: ×20. (F), predominant expression of IFNλ in a cellular crescent formation in the glomeruli (original magnifications: ×40) in a kidney biopsy from a patient with LN class IV. Agneta Zickert et al. Lupus Sci Med 2016;3:e000170 ©2016 by Lupus Foundation of America