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The programmed cell death-1 (PD-1)/programmed cell death ligand 1 (PD-L1) pathway is an important host immunosuppression mechanism. Soluble PD-1 (sPD-1) and PD-L1 (sPD-L1) expression regulates co-inhibitory signals in autoimmune disorders. Here, we evaluated whether serum sPD-1 and sPD-L1 is involved in immune dysfunction and assessed its relationship with SLE. Blood samples were obtained from 130 patients with SLE and 44 healthy controls. Serum sPD-1 and sPD-L1 were tested by enzyme-linked immunosorbent assay (ELISA). Relevant immune parameters were analyzed. Both serum sPD-1 and sPD-L1 were significantly higher in the SLE patients than in the controls. A series of severe disease clinical manifestations and laboratory features such as presence of decreased complement component 3, complement component 4 and SLEDAI > 8 were associated with elevated sPD-1 and sPD-L1. Our study suggests that abnormal sPD-1 and sPD-L1 expression may be involved in the imbalance of immune regulation in SLE. This article is protected by copyright. All rights reserved.Radiation is the most effective treatment for localized lymphoma, but treatment of multifocal disease is limited by toxicity. Radioimmunotherapy (RIT) delivers tumoricidal radiation to multifocal sites, further augmenting response by dose-escalation. This phase II trial evaluated high-dose RIT and chemotherapy prior to autologous stem-cell transplant (ASCT) for high-risk, relapsed or refractory (R/R) B-cell non-Hodgkin lymphoma (NHL). The primary endpoint was progression free survival (PFS). Secondary endpoints were overall survival (OS), toxicity, and tolerability. Patients age less then  60 years with R/R NHL expressing CD20 were eligible. Mantle cell lymphoma (MCL) patients could proceed to transplant in first remission. Patients received I-131-tositumomab delivered at ≤ 25Gy to critical normal organs, followed by etoposide, cyclophosphamide and ASCT. 107 patients were treated including aggressive lymphoma (N=29), indolent lymphoma (N=45), and MCL (N=33). After a median follow-up of 10.1 years, the 10-year PFS for the aggressive, indolent, and MCL groups were 62%, 64%, 43% respectively. The 10-year OS for the aggressive, indolent, and MCL groups were 61%, 71%, 48% respectively. Toxicities were similar to standard conditioning regimens and non-relapse mortality at 100 days was 2.8%. Late myeloid malignancies were seen in 6% patients. High-dose I-131-tositumomab, etoposide and cyclophosphamide followed by ASCT appeared feasible, safe, and effective in treating NHL, with estimated PFS at 10-years of 43-64%. In light of novel cellular therapies for R/R NHL, high-dose RIT-containing regimens yield comparable efficacy and safety and could be prospectively compared. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.Increasing prevalence of allergic and autoimmune diseases urges clinicians and researchers to search for new and efficient treatments. Strategies that activate antigen-specific immune tolerance and simultaneously maintain immune reactivity to all other antigens deserve special attention. Accordingly, antigen-presenting cells (APCs) seem to be the best suited for orchestrating these mechanisms by directing T cell immune responses toward a tolerant subtype. Recent advances in understanding cell-to-cell communication via extracellular vesicles (EVs) make the latter promising candidates for reprogramming APCs toward a tolerant phenotype, and for mediating tolerogenic APC function. Thus, comprehensive studies have been undertaken to describe the interactions of APCs and EVs naturally occurring during immune tolerance induction, as well as to develop EV-based maneuvers enabling the induction of immune tolerance in an antigen-specific manner. In this review, we summarize the findings of relevant studies, with a special emphasis on future perspectives on their translation to clinical practice. This article is protected by copyright. All rights reserved.The variations in human skin color mainly occur due to differences in the distribution of melanin pigment throughout the body; synthesised by epidermal melanocytes which are further taken up by keratinocytes present in epidermis. Recently, it has been discovered that besides these cells dermis derived fibroblast factors also play a prominent role in regulating skin pigmentation. There exists a signal cross-talk between epidermal melanocytes, keratinocytes and dermal fibroblasts and any impairment in these signaling pathways may give rise to pigmentary disorders. Vitiligo is a hypopigmentary disorder and alteration in the expression level of several fibroblast-specific factors has been reported in the lesional skin of vitiligo patients. In such patients, there is decrease in the expression levels of factors such as Basic Fibroblast Growth Factor (bFGF), Stem Cell Factor (SCF) and Keratinocyte Growth Factor (KGF) alongwith a steep increase in the expression levels of Dickkopf 1 (DKK1). Patients affected with hyperpigmentary disorder like melasma exhibit a marked increase in SCF and KGF expression levels leading to increase in melanin production and those affected with solar lentigo experience upregulation in the expression levels of SCF, KGF and HGF (Hepatocyte Growth Factor). find more Hence, we conlcude that new therapeutic strategies can be adopted to cure these pigmentary disorders by targeting factors involved in cross-talk signaling between epidermal melanocytes, keratinocytes and dermal fibroblasts. This article is protected by copyright. All rights reserved.In the daily clinical practice, many suspected spider bites can be caused by other conditions, decreasing diagnostic accuracy, such as methicillin-resistant Staphylococcus aureus infections, cutaneous anthrax, dermatomycosis, erysipelas, furuncles, streptococcal ecthyma, herpes virus, impetigo, Lyme disease, pyoderma gangrenosum, sporotrichosis, autoimmune vasculitis, chemical burns, diabetic ulcers, lymphomatoid papulosis, venous stasis ulcers and other arthropod bites and stings. This article is protected by copyright. All rights reserved.