Exclusive involvement of H-2D(b) or H-2K(d) product in the interaction between T-killer lymphocytes and syngeneic H-2(b) or H-2(d) viral lymphomas

It was demonstrated previously that the cytolysis of murine viral lymphoma cells by anti-murine sarcoma virus (MSV) syngeneic T-killer lymphocytes was restricted by some products of the H-2 complex. The respective role of the products of different regions of the H-2 complex were studied with six H-2(b) and three H-2(d) lymphomas induced by five different type C viruses. They were tested in a classical chromium release test against anti-MSV T-killer cells obtained from different inbred strains of mice, including several H-2 recombinants. Tumors o£ the H-2(b) haplotype were lysed only when effectors and target cells have in common the D(b) region. On the contrary an identity limited to the K end of the H-2 complex is necessary and sufficient in the H-2(d) haplotype. An in vitro restimulation of the spleen cells with concanavalin A strongly increased the activity of in vivo-primed T lymphocytes but did not provide any response for in vivo-primed but nonresponder cells. Preincubation of the tumor cells with anti-H-2 sera abolished the lysis by syngeneic anti-MSV effector lymphocytes. The same results were obtained by preincubating the H-2(b) targets with anti-H-2D(b), or the H-2(d) target with anti-H-2K(d). Preincubation with anti-H-2K(b) or anti- H-2D(d) were ineffective. These results show that the T-killer/target cells interaction in the MSV system involved some products of the H-2 complex which might be different with the various H-2 haplotypes and could possibly vary according to the antigenic specificity. A specific association of a viral product with a normal cellular structure, directed by the H-2 region during the viral budding could explain the observed results

Micrometer-Thin Crystalline-Silicon Solar Cells Integrating Numerically Optimized 2-D Photonic Crystals

A 2-D photonic crystal was integrated experimentally into a thin-film crystalline-silicon solar cell of 1-{\mu}m thickness, after numerical optimization maximizing light absorption in the active material. The photonic crystal boosted the short-circuit current of the cell, but it also damaged its open-circuit voltage and fill factor, which led to an overall decrease in performances. Comparisons between modeled and actual optical behaviors of the cell, and between ideal and actual morphologies, show the global robustness of the nanostructure to experimental deviations, but its particular sensitivity to the conformality of the top coatings and the spread in pattern dimensions, which should not be neglected in the optical model. As for the electrical behavior, the measured internal quantum efficiency shows the strong parasitic absorptions from the transparent conductive oxide and from the back-reflector, as well as the negative impact of the nanopattern on surface passivation. Our exemplifying case, thus, illustrates and experimentally confirms two recommendations for future integration of surface nanostructures for light trapping purposes: 1) the necessity to optimize absorption not for the total stack but for the single active material, and 2) the necessity to avoid damage to the active material by pattern etching.Comment: Authors' postprint version - Editor's pdf published online on Nov.

Absorbing photonic crystals for thin film photovoltaics

The absorption of thin hydrogenated amorphous silicon layers can be efficiently enhanced through a controlled periodic patterning. Light is trapped through coupling with photonic Bloch modes of the periodic structures, which act as an absorbing planar photonic crystal. We theoretically demonstrate this absorption enhancement through one or two dimensional patterning, and show the experimental feasibility through large area holographic patterning. Numerical simulations show over 50% absorption enhancement over the part of the solar spectrum comprised between 380 and 750nm. It is experimentally confirmed by optical measurements performed on planar photonic crystals fabricated by laser holography and reactive ion etching.Comment: 6 pages. SPIE Photonics Europe pape

Porous polymeric microparticles foamed with supercritical CO₂ as scattering white pigments

Nowadays, titanium dioxide (TiO2) is the most commercially relevant white pigment. Nonetheless, it is widely criticized due to its energy-intensive extraction and costly disposal of harmful by-products. Furthermore, recent studies discuss its potential harm for the environment and the human health. Environment-friendly strategies for the replacement of TiO2 as a white pigment can be inspired from nature. Here whiteness often originates from broadband light scattering air cavities embedded in materials with refractive indices much lower than that of TiO2. Such natural prototypes can be mimicked by introducing air-filled nano-scale cavities into commonly used polymers. Here, we demonstrate the foaming of initially transparent poly(methyl methacrylate) (PMMA) microspheres with non-toxic, inert, supercritical CO2. The properties of the foamed, white polymeric pigments with light scattering nano-pores are evaluated as possible replacement for TiO2 pigments. For that, the inner foam structure of the particles was imaged by phase-contrast x-ray nano-computed tomography (nano-CT), the optical properties were evaluated via spectroscopic measurements, and the mechanical stability was examined by micro compression experiments. Adding a diffusion barrier surrounding the PMMA particles during foaming allows to extend the foaming process towards smaller particles. Finally, we present a basic white paint prototype as exemplary application

A Crucial Role for Infected-Cell/Antibody Immune Complexes in the Enhancement of Endogenous Antiviral Immunity by Short Passive Immunotherapy

Antiviral monoclonal antibodies (mAbs) represent promising therapeutics. However, most mAbs-based immunotherapies conducted so far have only considered the blunting of viral propagation and not other possible therapeutic effects independent of virus neutralization, namely the modulation of the endogenous immune response. As induction of long-term antiviral immunity still remains a paramount challenge for treating chronic infections, we have asked here whether neutralizing mAbs can, in addition to blunting viral propagation, exert immunomodulatory effects with protective outcomes. Supporting this idea, we report here that mice infected with the FrCasE murine retrovirus on day 8 after birth die of leukemia within 4–5 months and mount a non-protective immune response, whereas those rapidly subjected to short immunotherapy with a neutralizing mAb survive healthy and mount a long-lasting protective antiviral immunity with strong humoral and cellular immune responses. Interestingly, the administered mAb mediates lysis of infected cells through an antibody-dependent cell cytotoxicity (ADCC) mechanism. In addition, it forms immune complexes (ICs) with infected cells that enhance antiviral CTL responses through FcγR-mediated binding to dendritic cells (DCs). Importantly, the endogenous antiviral antibodies generated in mAb-treated mice also display the same properties, allowing containment of viral propagation and enhancement of memory cellular responses after disappearance of the administered mAb. Thus, our data demonstrate that neutralizing antiviral mAbs can act as immunomodulatory agents capable of stimulating a protective immunity lasting long after the end of the treatment. They also show an important role of infected-cells/antibody complexes in the induction and the maintenance of protective immunity through enhancement of both primary and memory antiviral T-cell responses. They also indicate that targeting infected cells, and not just viruses, by antibodies can be crucial for elicitation of efficient, long-lasting antiviral T-cell responses. This must be considered when designing antiviral mAb-based immunotherapies

Kawasaki syndrome: an intriguing disease with numerous unsolved dilemmas

More than 40 years have passed since Kawasaki syndrome (KS) was first described. Yet KS still remains an enigmatic illness which damages the coronary arteries in a quarter of untreated patients and is the most common cause of childhood-acquired heart disease in developed countries. Many gaps exist in our knowledge of the etiology and pathogenesis of KS, making improvements in therapy difficult. In addition, many KS features and issues still demand further efforts to achieve a much better understanding of the disease. Some of these problem areas include coronary artery injuries in children not fulfilling the classic diagnostic criteria, genetic predisposition to KS, unpredictable ineffectiveness of current therapy in some cases, vascular dysfunction in patients not showing echocardiographic evidence of coronary artery abnormalities in the acute phase of KS, and risk of potential premature atherosclerosis. Also, the lack of specific laboratory tests for early identification of the atypical and incomplete cases, especially in infants, is one of the main obstacles to beginning treatment early and thereby decreasing the incidence of cardiovascular involvement. Transthoracic echocardiography remains the gold-standard for evaluation of coronary arteries in the acute phase and follow-up. In KS patients with severe vascular complications, more costly and potentially invasive investigations such as coronary CT angiography and MRI may be necessary. As children with KS with or without heart involvement become adolescents and adults, the recognition and treatment of the potential long term sequelae become crucial, requiring that rheumatologists, infectious disease specialists, and cardiologists cooperate to develop specific guidelines for a proper evaluation and management of these patients. More education is needed for physicians and other professionals about how to recognize the long-term impact of systemic problems related to KS