Imiquimod is an immune response modifier commercially available as a 3.75 and 5% cream. Topical imiquimod stimulates the innate and adaptive immune responses and induces cytokine production. This allows its use for the treatment of a wide variety of benign and malignant skin conditions due to its potential antiviral, antitumor, and immunoregulatory effects. Currently, topical imiquimod is US Food and Drug Administration (FDA)-approved for the treatment of anogenital warts, actinic keratosis, and superficial basal cell carcinomas. However, it has also shown a beneficial effect in the treatment of many other skin disorders. In this review, we describe existing evidence on the mechanism of action of topical imiquimod, its FDA-approved indications, off-label uses, and side effects.
Background and aims Vd2 T cells have predominantly been investigated in tumour immuno-surveillance and the host defense against viral invasion. The precise role of Vd2 T cells in the pathogenesis of SLE remains elusive. Methods We measured the proportion of peripheral Vd2 T cells as well as the status and chemokine receptor expression profiles in SLE patients and healthy control (HC). In addition, Vd2 T cell infiltration in the kidneys of patients with lupus nephritis was examined. Results The percentage of peripheral Vd2 T cells in new-onset SLE was decreased, and negatively correlated with the SLE Disease Activity Index score and the severity of proteinuria. These cells had a decreased apoptosis but an increased proliferation , and they showed increased accumulation in SLE kidneys. Moreover, IL-21 production and CD40L, CCR4, CCR7, CCR8, CXCR1 and CX3CR1 expression in Vd2 T cells from SLE patients was significantly higher than from HC (p<0.05), and these factors were down-regulated in association with the repopulation of peripheral Vd2 T cells in patients who were in remission (p<0. Background and aims Systemic Lupus Erythematosus (SLE) is associated with an increased IFN gene signature detectable in the peripheral blood. Plasmacytoid dendritic cells (pDC) are potent producers of IFNa in response to TLR9 and TLR7-agonists. pDCs which express high levels of CD123 (IL-3Ra) can be depleted by JNJ-56022473 (JNJ-473), a novel Fc-engineered neutralising and depleting therapeutic antibody targeting CD123. Methods We investigated the effects of pDC depletion with JNJ-473 on IFNa production and gene expression within SLE patient PBMC (n=8) stimulated with TLR-agonists, SLE-immune complexes (IC, SLE IgG with necrotic cell lysates (NCL)) and sera from SLE patients with NCL. Results Stimulation with CpGc, SLE-IC or SLE sera was able to induce high levels of IFNa, which was greatly decreased by pDC depletion with JNJ-473. SLE-IC and SLE sera stimulation also induced the differential expression of hundreds of genes and could induce similar genes to TLR9-agonism. pDC depletion with JNJ-473 prevented the upregulation of TLR9-induced genes. JNJ-473 conferred minimal effects on the induction of genes in response to the TLR4-agonist LPS. Furthermore , a distinct 11-gene IFN signature was induced by CpGc and SLE-IC that was significantly reduced by treatment with JNJ-473, suggesting that the depletion of pDCs with JNJ-473 could have distinct and specific effects on the detectable IFN signature in many SLE patients. Conclusions Depletion of pDCs with JNJ-473 is able to dramatically decrease IFNa production and IFN gene signature induced by TLR9-agonists and SLE-IC. Background and aims Glucocorticoid-induced Leucine Zipper (GILZ) is a GC-inducible gene with multiple immune-regulatory functions, and GILZ deficiency in mice results in the development of a lupus-like phenotype. In Systemic Lupus Erythematosus (SLE), plasmacytoid dendritic cells (pDCs) are major producers of Type 1 interferons (IFN) in response to nucleic acid-containin...
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