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Stroke causes systemic immunosuppression. T lymphocytes are involved in infarct size in the early stages of stroke. However, the phenotypes of T lymphocytes and their functions in peripheral immune organs and the brain have not been well analyzed in the acute and chronic phases of stroke. Here, we investigated pathological phenotypic alterations in the systemic immune response, especially changes in T lymphocytes, from one day to six months after ischemic stroke in mice. Impairment in thymocyte numbers, development, proliferation, and apoptosis were observed for up to two weeks. The number of mature T cells in the spleen and blood decreased and showed reduced interferon-γ production. Increased numbers of CD4-CD8-CD3+ double-negative T cells were observed in the mouse brain during the early stages of stroke, whereas interleukin (IL)-10+Foxp3+ regulatory T lymphocytes increased from two weeks during the chronic phase. These phenotypes correlated with body weight and neurological severity scores. The recovery of T lymphocyte numbers and increases in IL-10+Foxp3+ regulatory T lymphocytes may be important for long-term neurological outcomes. Dynamic changes in T lymphocytes between the acute and chronic phases may play different roles in pathogenesis and recovery. This study provides fundamental information regarding the T lymphocyte alterations from the brain to the peripheral immune organs following stroke.

Prostaglandin E2 (PGE2) is widely recognized as one of the major bioactive lipids that, with the striking regenerative potential, promote drug-resistance in cancer cells as well as immune evasion in the tumor microenvironment (TME). Primarily driven by apoptotic cell death, PGE2 is thought to elicit wound-healing responses to help provide an immunosuppressive and proliferative niche that supports cancer stem cell repopulation and thereby therapy-resistance. While COX1/2 inhibitors that attenuate PGE2 production have shown promising anti-cancer effects in various (pre-)clinical settings, the gastrointestinal- and cardiotoxicities precluded their development as anti-cancer agents. It is anticipated that specific targeting of PGE2 signaling via its cognate receptors constitutes a safer and potentially more effective approach. Of the receptor subtypes EP1-4, Gα,s-coupled EP2 and EP4 are believed to be directly involved in immunosuppressive effects of PGE2.OCT-598 is a novel, highly potent and selective EP2/EP4 dual antagonist with Ki values of 23 nM and 0.2 nM vs EP2 and EP4, respectively. PGE2 inhibited normal differentiation of human monocytes into CD1a+CD16- dendritic cells under the presence of GM-CSF and IL-4 and promoted differentiation towards CD1a-CD16+ macrophages in vitro. However, EP2/EP4 dual inhibition by OCT-598 reversed this phenomenon to a greater extent than either EP2- or EP4-specific inhibitor alone. In vivo, OCT-598 effected tumor growth inhibition in multiple syngeneic mouse models as a single agent as well as in combination with an immune checkpoint blocker (ICB). Furthermore, the addition of OCT-598 to the lung cancer standard-of-care regimen (anti-PD-1 plus chemotherapy) in TC-1 mouse lung adenocarcinoma model gave rise to complete tumor regression. In conclusion, dual blockade of EP2 and EP4 by OCT-598 is shown to be a compelling strategy to reinforce antitumor effects by thwarting PGE2-mediated therapy resistance and immune evasion.Findings from this study provide a rationale for clinical development of OCT-598 as a therapeutic option for human malignant cancers. Citation Format: Youngrae Lee, Sujeong Baek, Dong Kwon Kim, Yeri Lee, Donggeon Kim, Seongin Jo, Sang Kyun Lim, Young Sook Shin, Soonsang Kwon, Seung Min Yang, Young Taek Kim, Seong-San Kang, Chun-Bong Synn, Kwangmin Na, Mi Hyun Kim, Heekyung Han, Yu Jin Han, Sungwoo Lee, Jae Hwan Kim, Mi Ran Yun, Youngseon Byeon, Young Seob Kim, Ji Yun Lee, Jii Bum Lee, Chang Gon Kim, Min Hee Hong, Sun Min Lim, Kyoung-Ho Pyo, Byoung Chul Cho, Taeyoung Yoon. OCT-598, a novel EP2/EP4 dual antagonist, promotes anti-tumor immune responses in syngeneic mouse tumor models in combination with standard-of-care chemo- and immunotherapies [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3234.

Heterogeneity in resistant to immunotherapies of tumor microenvironment (TME) has been implicated in immunotherapies to cause immune evasion or drug resistance. This study was conducted to explore the heterogeneity of TME through multiplex IHC, spatial and RNA sequencing analysis. We selected a sample from a lung adenocarcinoma patient without EGFR-activating mutation and expressing 30% of PD-L1. For quantitative analysis by multiplex IHC, various markers including CD4, CD8, FoxP3, granzyme B, CD20 and pan-cytokeratin were stained with 7 different fluorescence dyes, which was imaged with Vectra Polaris (Akoya). For scRNAseq and spatial RNAseq, we used 5’ chromium library kit (10X Genomics) to make library construction. Integrated raw data was generated using Cell ranger, Seurat pipeline and Azimuth package. The tumor area was divided into 16 clusters in which we selected 2 clusters based on CD3/45 expression. There was a noticeable distinction between the two clusters which were defined as the ‘High’ region (CD45highCD3high cluster) and the ‘Low’ region (CD45lowCD3low cluster). By multiplex IHC, percentage of CD8+T cells was higher in the ‘High’ region than in the ‘Low’ region (8.5% vs. 0.8%, respectively). Subsequent analysis of two clusters using spatial and single cell RNA seq, the ‘Low’ region was characterized by increased hypoxia-associated gene expressions including HIF1A, HIF3A and VEGFA. Various immune cells were abundant in the ‘High’ region and CD45 expression level was 11-fold higher in the ‘High’ region compared to the ‘Low’ region. Cytokine/chemokine network analysis via spatial RNAseq revealed that gene expression of tumor necrosis factor (TNF) family-associated factors increased in the 'High' region compared to the ‘Low’ region (TNF, FAS, TRAIL, RANKL and CD40), which is well-known to promotes apoptosis, programmed cell death, or necrosis of certain cancer. Additionally, the ‘High’ region also had elevated levels of the PD-1/PD-L1, CD155, CD122/TIGIT, Siglec10/CD24, LAG3/LAGLS3, and CD47/CD172a axes, suggesting active immune responses. Intriguingly, combined analyses showed that ‘High’ region showed enhanced level of CD44 expression as the leading-edged gene, which suggests the metastatic potential of tumor cells. Furthermore, scRNA analysis confirmed that CD44 expression was mainly higher in macrophages, suggesting that tumor-associated macrophages partially affected tumor cell metastasis in the ‘High’ region. Our finding suggests that understanding the intratumoral immunological heterogeneity of lung adenocarcinoma can help to study the mechanism of tumor heterogeneity by integrated spatial RNAseq and scRNAseq analyses. This type of technique could be applied to understand complex networks of anti-tumor immune activities, drug resistance mechanisms and immunotherapeutic response of cancer. Citation Format: Seul Lee, Jae-Hwan Kim, Kwangmin Na, Seung Min Yang, Dong Kwon Kim, Sujeong Baek, Seong-san Kang, Yu Jin Han, Chun-Bong Synn, Mi hyun Kim, Heekyung Han, Young Taek Kim, Sungwoo Lee, Youngseon Byeon, Young Seob Kim, Ji Yun Lee, Jii Bum Lee, Chang Gon Kim, Min Hee Hong, Sun Min Lim, Kyoung-Ho Pyo, Byoung Chul Cho. Characterization of immunological heterogeneity in the tumor microenvironment by integrated analyses using single cell RNAseq, spatial RNAseq and multiplex IHC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6780.

Background: The Aryl hydrocarbon receptor (AhR) is one of the most predominant regulators of cancer metabolism. The AhR exerts important immunosuppressive functions by activating Treg cells and myeloid-derived suppressor cells and repressing CD8+ effector T cells. Here, we propose that a best-in-class AhR inhibitor, DA-4505, improves anti-tumor efficacy via modulation of tumor immune surveillance compared to BAY2416964, an AHR antagonist drug candidate being studied in the clinical phase. Methods: To evaluate anti-tumor effects of DA-4505 and BAY2416964, the two AhR inhibitors were dosed at 10 mg/kg once daily alone or in combination with aPD-1 (10 mg/kg) in surgical and chemotherapy models, and a PDX model (YHIM2004). Tumor volume, relapse, and survival were evaluated, and immune profiles were analyzed with IHC, flow cytometry, and scRNAseq. Results: A significant tumor reduction appeared in the CT26 and 4T1 tumor models after the DA-4505 treatment compared to vehicle group (P Conclusion: The AhR inhibitor DA-4505 demonstrated an improvement in anti-tumor efficacy. In addition, it has shown a synergistic effect when combined with aPD-1. Discoveries from this study provide a preclinical rationale for future clinical implications in solid tumor. Citation Format: DongKwon Kim, Sujeong Baek, Seung Min Yang, Yu Jin Han, Seong-san Kang, Chun-Bong Synn, Mi Hyun Kim, Heekyung Han, Kwangmin Na, Young Taek Kim, Sungwoo Lee, Taedong Han, Hyounmie Doh, Jongho Cho, Dajeong Kim, Daewon Cha, Jae Hwan Kim, Youngseon Byeon, Young Seob Kim, Mi Ran Yun, Ji Yun Lee, Jii Bum Lee, Chang Gon Kim, Min Hee Hong, Sun Min Lim, Byoung Chul Cho, Kyoung-Ho Pyo. A novel AhR inhibitor ‘DA-4505’ improved the anti-cancer efficacy of surgical and chemotherapy via synergistic anti-tumor effects of aPD-1. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5107.

Introduction: Unmet needs exist for immunotherapy targeting PD-1/PD-L1 in head and neck squamous cell carcinoma (HNSCC) and lung squamous cell carcinoma (LUSC) due to its suboptimal response. Amivantamab, a bispecific antibody targeting epidermal growth factor receptor (EGFR) and c-Met, has been demonstrated to induce antibody-dependent cytotoxicity and trogocytosis in tumor cells. We hypothesized that combination of amivantamab with pembrolizumab may synergistically enhance antitumor immunity. In this study, we present comprehensive immunomodulatory and synergistic antitumor efficacy of amivantamab and pembrolizumab in humanized HNSCC and LUSC mice models. Methods: EGFR and MET-expressing tumors from a HNSCC and a LUSC patient were transplanted into Hu-CD34-NSG to establish humanized patient-derived xenograft (PDX) models. Tumor-bearing PDXs were treated with vehicle, pembrolizumab (10mpk, Q5D, n=10), amivantamab (10mpk, BIW, n=10), or a combination of pembrolizumab and amivantamab (n=10). Analysis of immune modulatory responses within the tumor microenvironment (TME) using multiplexed IHC, flow cytometry, and single cell RNA sequencing was performed. Results: Combination of amivantamab and pembrolizumab showed a significant reduction of tumor volume (p Conclusion: Our study demonstrated combinatorial benefits of amivantamab and pembrolizumab by effectively remodeling TME, providing a preclinical rationale to clinically combine amivantamab and PD-1 blockade treatments. Citation Format: Sun Min Lim, Chun-Bong Synn, Seong-san Kang, DongKwon Kim, Soo-Hwan Lee, Sujeong Baek, Seung Min Yang, Yu Jin Han, Mi hyun Kim, Heekyung Han, Kwangmin Na, Young Taek Kim, Sungwoo Lee, Mi Ran Yun, Jae Hwan Kim, Youngseon Byeon, Young Seob Kim, Jii Bum Lee, Ji Yun Lee, Chang Gon Kim, Min Hee Hong, Kyoung-Ho Pyo, Joshua Curtin, Bharvin Patel, Isabelle Bergiers. Combinatorial activity of amivantamab and pembrolizumab in head and neck squamous cell carcinoma and lung squamous cell carcinoma expressing wild-type EGFR and MET [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5865.

Additional file 7. Macrophage polarization in hyperinflammation model.

Additional file 5. Proinflammatory cytokine expression in in vitro model of hyperinflammation and immunosuppression.

Additional file 4. Oxygen consumption trace in organ of cecal slurry model in rat.

Additional file 1. Respiratory control rates of mitochondria in the rat sepsis model. Respiratory control rates were measured in spleen, muscle, liver and kidney tissues both before and after induction of sepsis.

Additional file 3. Distributions of transplanted mitochondria in septic spleens.

Additional file 6. Proinflammatory cytokine expression in in vitro model of hyperinflammation and immunosuppression with ETC inhibitors.

Additional file 8. Phagocytosis of E.coli-FITC in immune paralysis model.

Additional file 2. Characterization of isolated mitochondria from L6 cells and UC-MSCs.

Background Sepsis has a high mortality rate, but no specific drug has been proven effective, prompting the development of new drugs. Immunologically, sepsis can involve hyperinflammation, immune paralysis, or both, which might pose challenges during drug development. Recently, mitochondrial transplantation has emerged as a treatment modality for various diseases involving mitochondrial dysfunction, but it has never been tested for sepsis. Methods We isolated mitochondria from L6 muscle cells and umbilical cord mesenchymal stem cells and tested the quality of the isolated mitochondria. We conducted both in vivo and in vitro sepsis studies. We investigated the effects of intravenous mitochondrial transplantation on cecal slurry model in rats in terms of survival rate, bacterial clearance rate, and the immune response. Furthermore, we observed the effects of mitochondrial transplantation on the immune reaction regarding both hyperinflammation and immune paralysis. To do this, we studied early- and late-phase cytokine production in spleens from cecal slurry model in rats. We also used a lipopolysaccharide (LPS)-stimulated human PBMC monocyte model to confirm the immunological effects of mitochondrial transplantation. Apoptosis and the intrinsic apoptotic pathway were investigated in septic spleens. Results Mitochondrial transplantation improved survival and bacterial clearance. It also mitigated mitochondrial dysfunction and apoptosis in septic spleens and attenuated both hyperinflammation and immune paralysis in the spleens of cecal slurry model in rats. This effect was confirmed with an LPS-stimulated human PBMC study. Conclusions In rat polymicrobial cecal slurry model, the outcome is improved by mitochondrial transplantation, which might have an immunomodulatory effect.

BackgroundT lymphocytes are involved in infarct size at the early stage of stroke. However, the phenotypes of T lymphocytes and their functions in peripheral immune organs and the brain have not been well-analyzed from the acute to the chronic phase of stroke.MethodsA 45 min transient middle cerebral artery occlusion mouse model was used. The phenotypes of T lymphocytes in the thymus, spleen, blood, and brain were determined using the neurological severity score (NSS) and body weights during the 6-month follow-up. ResultsImpairment of thymocyte numbers, development, proliferation, and apoptosis was observed for up to 2 weeks. The number of mature T cells in the spleen and blood decreased and showed less interferon- production for up to 2 weeks. Increased numbers of CD44+CD62L- effector T cells and CD4-CD8-CD3+ double negative T cells were observed in mouse brains in the early phase of stroke, while interleukin (IL)-10+Foxp3+ regulatory T cell levels increased for 1 week during the chronic phase. These phenotypes were correlated with body weight and the NSS. Conclusions The recovery of T lymphocyte numbers and increased IL-10+Foxp3+ regulatory T lymphocytes may be important for the improvement of long-term neurological outcomes. Dynamic changes in T lymphocytes from the acute and chronic phase may play different roles, such as pathological and recovery roles, respectively. This study provides fundamental information regarding the T lymphocyte alterations from the brain to the peripheral immune organs from the acute to the chronic phase of stroke.

Atopic dermatitis (AD) is a chronic inflammatory skin disease. A hallmark of AD is dry itchy skin that results from defects in the epidermal barrier function. Aloe vera is used widely to promote general health and is administered topically to treat skin conditions such as eczema, burns and wounds. However, effects of A vera on AD were not fully elucidated. In this study, we investigated the oral administration of processed A vera gel (PAG) containing low molecular weight Aloe polysaccharides to treat ovalbumin (OVA)-induced AD in mice. Oral administration of PAG suppressed total and OVA-specific IgE production in sera and decreased the epidermal thickness of skin. Numbers of Ki-67-positive cells were reduced by PAG treatment. Expression levels of tight junction genes, including those that encode ZO-1, Claudin-1 and Claudin-8, were decreased in AD skin lesions, whereas oral administration of PAG partially restored the expression levels of tight junction genes. In addition, IL-4 and IL-17A mRNA transcript levels were reduced in skin lesions after PAG treatment. Taken together, our findings suggest that oral administration of PAG ameliorated AD, normalized tight junction gene expression and suppressed inflammatory cytokines in AD skin.

There is a great demand for the development of self-powered physical sensors for wearable applications in recent years. However, it is still challenging to achieve self-powered sensors with a high stability, accuracy, and linearity. Here, a novel wearable self-powered pressure sensor based on the integration of a piezo-transmittance microporous elastomer (PTME) and a thin-film organic solar cell (OSC) is proposed. In contrast to the sensors based on other mechanisms such as piezoelectricity or triboelectricity, the proposed self-powered pressure sensor is cable of measuring static pressure continuously and stably, and utilizes the ambient light as the power source regardless of its intensity. The PTME shows the light transmittance changes by a gradual closure of micropores with compression in response to the applied pressure. This unique optical characteristics of the PTME enables the OSC to generate varying electrical current in response to the pressure. The proposed self-powered pressure sensor shows a high-performance with a sensitivity of 0.101/kPa, a linearity of R2 = 0.995, and fast and reversible response to the pressure up to ~100 kPa. As practical applications of the proposed sensor, a detection of flexion/extension of a human finger for the manipulation of a prosthetic robot finger and a wind detection for the continuous monitoring of the wind speed and direction have been demonstrated.

This paper reports a flexible optical pressure sensor based on a porous structured elastomer and its application to a wearable human motion detecting device, which is operated in a self-power-generating way by integrating with an organic photovoltaic cell. Complete investigation of material characteristics and sensing performances as well as optical simulation for understanding the sensing mechanism have been produced. Finally, a self-power-generating wearable motion sensing device was demonstrated as a sensor for detection of flexion and extension motion of a human finger.

This paper reports a novel flexible optical pressure sensor based on a porous elastomer film as a light transmission medium with ultra-high sensitivity and simplicity. The pore-closing behavior under external pressure and corresponding change of light transmittance of porous elastomer film were investigated. The porous elastomer film based optical pressure sensor showed highly sensitive and stable performance with the sensitivity of 2.177 kPa−1 over the pressure range of 0–10 kPa. Finally, the optical pressure sensor was integrated with thin film solar cell to modulate the generated electrical current towards self-powered sensing platform.

We have developed a self-powered gas sensor operating without external power under a light source, unlike a sensor that requires an external power source, such as a chemiresistive gas sensor or an electrochemical gas sensor. The sensor consists of a colorimetric film and an organic solar cell. The sensor uses a color change caused by the reaction of the N, N,N',N'-tetramethyl-p-phenylenediamine (TMPD) with NO 2 gas. The color change caused by the redox reaction of the colorimetric material does not require a separate light source and photodetector, unlike the conventional colorimetric sensor, because it directly changes the output of the solar cell by changing the transmittance of the film. Using this sensor, 1, 5, 10, 20ppm NO 2 gas was detected without external power source, and the performance of the gas sensor could be improved by using microstructure. This work is the first demonstration of self-powered gas sensor based on the combination of photovoltaic cell and microstructured colorimetric film.

BACKGROUND Anti-interleukin-33 (anti-IL-33) and anti-Siglec-F antibodies have potent anti-allergic effects on murine allergic asthma and rhinitis and induce eosinophil apoptosis. OBJECTIVE We aimed to determine whether post-sensitization with anti-IL-33/anti-Siglec-F treatments exhibited more potent effects compared to individual treatments in a murine allergic asthma model. MATERIAL AND METHODS Twenty-five BALB/c mice were separated into five groups (n = 5): Group A (control), Group B (ovalbumin [OVA] challenge), Group C (OVA + anti-IL-33), Group D (OVA + anti-Siglec-F), and Group E (OVA + anti-IL-33 + anti-Siglec-F). Serum total/ OVA-specific IgE, bronchoalveolar lavage (BAL) inflammatory cells and cytokines (IL-4 and IL-5), histopathological lung properties, and airway hyperreactivity were compared. RESULTS Ovalbumin challenge induced strong immune and inflammatory responses with > 6-fold IgE level increases; 10- to 25-fold BAL eosinophil, neutrophil, and lymphocyte count increases; and > 1.5-fold IL-4 and IL-5 level increases (p < 0.05). Whereas anti-IL-33 reduced neutrophil counts, anti-Siglec-F and anti-IL-33/anti-Siglec-F reduced both eosinophil and neutrophil counts (p < 0.05). Individual treatments reduced OVA-mediated bronchiolar infiltration by 50% (p

Background Sialic acid-binding Ig-like lectin-F (Siglec-F) in mice and its functional paralog Siglec-8 in humans are transmembrane receptors that play a role in the apoptosis of eosinophils. We aimed to evaluate the therapeutic potential of anti-Siglec-F antibodies in a murine model of allergic rhinitis. Methods Twenty-eight BALB/c mice were used. In group A (control group, n = 7), mice were sensitized and challenged with saline. In group B (ovalbumin [OVA] challenge group, n = 7), OVA was used for i.p. sensitization and intranasal challenge. Mice in group C (control IgG group, n = 7) or those in group D (anti-Siglec-F group, n = 7) had been given rabbit control IgG or anti-Siglec-F antibody injections, respectively. We assessed the number of nose-scratching events; serum total/OVA-specific IgE; the number of eosinophils, neutrophils, and lymphocytes in bronchoalveolar lavage (BAL) fluid; histopathological changes in nasal cavity tissues; and the levels of IL-4, IL-5, and IL-13 in BAL fluid. Results Mice in group D had significantly less nose scratching. Serum total and OVA-specific IgE were not significantly changed. The number of eosinophils in BAL fluid and in the lamina propria of the nasal cavity mucosa was significantly decreased with anti-Siglec-F antibody treatment. The levels of Th2 cytokines such as IL-4, IL-5, and IL-13 were also significantly decreased with anti-Siglec-F antibody treatment. Conclusion Anti-Siglec-F antibody has beneficial effects in a mouse model of experimental allergic rhinitis.

Mesenchymal stromal cells (MSCs) are known to suppress T-cell activation and proliferation. Several studies have reported that MSCs suppress CD25 expression in T cells. However, the molecular mechanism underlying MSC-mediated suppression of CD25 expression has not been fully examined. Here, we investigated the mTOR pathway, which is involved in CD25 expression in T cells. We showed that MSCs inhibited CD25 expression, which was restored in the presence of an inducible nitric oxide synthase (iNOS) inhibitor. Since CD25 mRNA expression was not inhibited, we focused on determining whether MSCs modulated components of the mTOR pathway in T cells. MSCs increased the phosphorylation of liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK) and decreased the phosphorylation of ribosomal protein S6 kinase 1 (S6K1) and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1). In addition, the expression of 4E-BP1 increased dramatically in the presence of MSCs. An m7GTP pull-down assay showed increased binding of 4E-BP1 to the 5′ cap-binding eukaryotic translation initiation factor 4E (eIF4E) complex in the presence of MSCs, which resulted in inhibition of mRNA translation. Treatment with 4EGI-1, a synthetic inhibitor of mRNA translation, also reduced CD25 expression in T cells. Polysome analysis confirmed decreased CD25 mRNA in the polysome-rich fraction in the presence of MSCs. Taken together, our results showed that nitric oxide, produced by MSCs, inhibits CD25 translation through regulation of the LKB1-AMPK-mTOR pathway to suppress T cells.

A novel self-charging platform is proposed using colloidal-quantum-dot (CQD) photovoltaics (PVs) via the near-infrared (NIR) band for low-power electronics. Low-bandgap CQDs can convert invisible NIR light sources to electrical energy more efficiently than wider spectra because of reduced thermalization loss. This energy-conversion strategy via NIR photons ensures an enhanced photostability of the CQD devices. Furthermore, the NIR wireless charging system can be concealed using various colored and NIR-transparent fabric or films, providing aesthetic freedom. Finally, an NIR-driven wireless charging system is demonstrated for a wearable healthcare bracelet by integrating a CQD PVs receiver with a flexible lithium-ion battery and entirely embedding them into a flexible strap, enabling permanent self-charging without detachment.

Most of the high-performance all-polymer solar cells (all-PSCs) reported to date are based on polymer donor and polymer acceptor pairs with largely overlapped light absorption properties, which seriously limits the efficiency of all-PSCs. This study reports the development of a series of random copolymer donors possessing complementary light absorption with the naphthalenediimide-based polymer acceptor P(NDI2HD-T2) for highly efficient all-PSCs. By controlling the molar ratio of the electron-rich benzodithiophene (BDTT) and electron-deficient fluorinated-thienothiophene (TT-F) units, a series of polymer donors with BDTT:TT-F ratios of 1:1 (P1), 3:1 (P2), 5:1 (P3), and 7:1 (P4) are prepared. The synthetic control of polymer composition allows for precise tuning of the light absorption properties of these new polymer donors, enabling optimization of light absorption properties to complement those of the P(NDI2HD-T2) acceptor. Copolymer P1 is found to be the optimal polymer donor for the fullerene-based solar cells due to its high light absorption, whereas the highest power conversion efficiency of 6.81% is achieved for the all-PSCs with P3, which has the most complementary light absorption with P(NDI2HD-T2).

Background Anti-interleukin-33 (anti-IL-33) and anti-Siglec-F antibodies have potent anti-allergic effects on murine allergic asthma and rhinitis and induce eosinophil apoptosis. Objective We aimed to determine whether post-sensitization with anti-IL-33/anti-Siglec-F treatments exhibited more potent effects compared to individual treatments in a murine allergic asthma model. Material and methods Twenty-five BALB/c mice were separated into five groups (n = 5): Group A (control), Group B (ovalbumin [OVA] challenge), Group C (OVA + anti-IL-33), Group D (OVA + anti-Siglec-F), and Group E (OVA + anti-IL-33 + anti-Siglec-F). Serum total/ OVA-specific IgE, bronchoalveolar lavage (BAL) inflammatory cells and cytokines (IL-4 and IL-5), histopathological lung properties, and airway hyperreactivity were compared. Results Ovalbumin challenge induced strong immune and inflammatory responses with > 6-fold IgE level increases; 10- to 25-fold BAL eosinophil, neutrophil, and lymphocyte count increases; and > 1.5-fold IL-4 and IL-5 level increases (p < 0.05). Whereas anti-IL-33 reduced neutrophil counts, anti-Siglec-F and anti-IL-33/anti-Siglec-F reduced both eosinophil and neutrophil counts (p < 0.05). Individual treatments reduced OVA-mediated bronchiolar infiltration by 50% (p

Mesenchymal stem cells (MSCs) possess immunomodulatory activities, including suppression of T-and B-cell activation. However, their effects on atopic dermatitis (AD) have not yet been studied. Using an ovalbumin-induced AD mouse model, we investigated whether MSCs can be used as therapeutics in AD. We isolated both allogeneic and syngeneic clonal MSCs (cMSCs) from mouse bone marrow according to the subfractionation culturing method. Our cMSCs suppressed both T-and B-cell activation. T-cell proliferation and cytokine production, including interferon (IFN)-gamma and interleukin (IL)-4, were suppressed by inhibition of transcription factors, such as T-bet, GATA-3, and c-Maf. Those transcription factors were nitric oxide dependent. Immunoglobulin E (IgE) suppression occurred through downregulation of AID and BLIMP-1, important regulators for isotype class switch and B-cell differentiation. The cMSCs were injected intravenously into ovalbumin-induced AD mouse model, and the therapeutic effects were analyzed. Injection of both allogeneic and syngeneic cMSCs in an AD mouse model inhibited cell infiltration in skin lesions and decreased the serum level of IgE. IL-4 expression was also suppressed by cMSCs in both the lymph node and skin. The cMSCs migrated to skin lesions and draining lymph nodes. Taken together, these data demonstrated that cMSCs, which suppressed T-and B-cell functions, can be used for the treatment of AD in mice.

Mesenchymal stem cells (MSCs) can perform immunomodulatory activities, including suppression of T- and B-cell proliferation. MSCs have been primarily studied for their suppression of pro-inflammatory Th1 responses, but their therapeutic effects on atopic dermatitis (AD), which is a Th2-dominant disease, have not been reported. In this study, using an ovalbumin-induced mouse AD model, we investigated whether MSCs reduce the allergic inflammation in AD. We used mouse bone marrow-derived clonal mesenchymal stem cells (mcMSCs) isolated by our newly established isolation protocol termed the subfractionation culturing method (SCM). When injected intravenously into animals between antigen challenges, mcMSCs were found to inhibit the majority of AD-specific pathological changes by decreasing cell infiltration in skin lesions and reducing serum level of IgE. To explore the mechanism of this effect, we investigated the effects of mcMSCs on IgE production in B cells. We found that mcMSCs significantly inhibited IgE production when B cells were stimulated either by lipopolysaccharide (LPS) or anti-CD40 antibodies in the presence of interleukin (IL)-4. In addition, allogeneic mcMSCs can inhibit both isotype class switching and terminal differentiation of B cells probably by inhibiting NF-κB activation. These results suggest that mcMSC-based cell therapy is a promising therapeutic modality for AD treatment.