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Despite recent advances in asthma treatments, the search for novel therapies remains necessary because there are still patients with recurrent asthma exacerbations and poor responses to the existing treatments. Since group 2 innate lymphoid cells (ILC2) play a pivotal role in asthma by triggering and exacerbating type 2 inflammation, controlling ILC2s function is key to combating severe asthma. Mucosal-associated invariant T (MAIT) cells are innate-like T cells abundant in humans and are activated both in a T cell receptor-dependent and -independent manner. MAIT cells are composed of MAIT1 and MAIT17 based on the expression of transcription factors T-bet and RORγt, respectively. MAIT cells play pivotal roles in host defense against pathogens and in tissue repair and are essential for the maintenance of immunity and hemostasis. Our recent studies revealed that MAIT cells inhibit both ILC2 proliferation and functions in a mouse model of airway inflammation. MAIT cells may alleviate airway inflammation in two ways, by promoting airway epithelial cell barrier repair and by repressing ILC2s. Therefore, reagents that promote MAIT cell-mediated suppression of ILC2 proliferation and function, or designer MAIT cells (genetically engineered to suppress ILC2s or promote repair of airway damage), may be effective therapeutic agents for severe asthma.

Blau syndrome (BS), is an autoinflammatory granulomatosis disease characterized by a distinct triad of skin, joint, and eye disorders similar to those of sarcoidosis, but the lung involvement frequently observed in sarcoidosis are rare. Granulomas from patients with BS displayed a distinct morphology indicating an exuberant chronic inflammatory response. Patients with BS may have granulomatous lung lesions, which require early diagnosis. To determine whether therapeutic intervention is needed for lung lesions, examining transbronchial lung cryobiopsy specimens and accumulating cases of BS with lung involvement could be contributed to improving BS management in the future.

Systemic administration of corticosteroids is used in the treatment of chronic eosinophilic pneumonia (CEP). However, in patients with CEP as well as other comorbidities, the adverse effects of corticosteroids should be minimized as much as possible. A 71-year-old woman was presented with aggravating asthma with CEP and sinusitis, and she had uncompensated liver cirrhosis (LC) with a Child-Pugh score of 7. Initial treatment with a low dose of oral corticosteroids (OCSs) in combination with tezepelumab, an anti-thymic stromal lymphopoietin (TSLP) antibody, resulted in rapid improvement of asthma and CEP without deteriorating LC. Sinusitis also improved after ceasing OCS. This case suggested that tezepelumab may be useful as a treatment option for patients with CEP, especially those with liver dysfunction.

Abstract This study investigated the utility of periostin, a matricellular protein, as a prognostic biomarker in patients with idiopathic pulmonary fibrosis (IPF) who received nintedanib. Monomeric and total periostin levels were measured by enzyme-linked immunosorbent assay in 87 eligible patients who participated in a multicenter prospective study. Forty-three antifibrotic drug-naive patients with IPF described in previous studies were set as historical controls. Monomeric and total periostin levels were not significantly associated with the change in forced vital capacity (FVC) or diffusing capacity of the lungs for carbon monoxide (DLCO) during any follow-up period. Higher monomeric and total periostin levels were independent risk factors for overall survival in the Cox proportional hazard model. In the analysis of nintedanib effectiveness, higher binarized monomeric periostin levels were associated with more favorable suppressive effects on decreased vital capacity (VC) and DLCO in the treatment group compared with historical controls. Higher binarized levels of total periostin were associated with more favorable suppressive effects on decreased DLCO but not VC. In conclusion, higher periostin levels were independently associated with survival and better therapeutic effectiveness in patients with IPF treated with nintedanib. Periostin assessments may contribute to determining therapeutic strategies for patients with IPF.

A 58-year-old man who had inhaled acetylene while welding 2 and 4 days previously and subsequently developed cough, dyspnea, and fever was referred by his general practitioner. A computed tomography scan showed diffuse ground-glass opacities in both lungs, and bronchoalveolar lavage fluid showed an increased proportion of eosinophils (25 %). Acute eosinophilic pneumonia (AEP) was diagnosed. Inhalation of acetylene was considered to be the most likely cause of AEP. Respiratory symptoms improved rapidly with intravenous corticosteroids. This is a rare case of AEP caused by inhalation of acetylene.

A 76-year-old woman was diagnosed with mucosa-associated lymphoid tissue (MALT) lymphoma by upper gastrointestinal endoscopy. She underwent further investigation for concomitant bilateral pleural effusions and right pulmonary consolidation. MALT lymphoma with the t(11; 18)(q21; q21) translocation and API2-MALT1 were detected in pleural fluid. Lymphoma was not histopathologically diagnosed by lung biopsies, but the same translocation was identified in bronchial lavage. MALT lymphoma is often difficult to diagnose by bronchoscopy because of only mild dysplasia. However, present report on using chromosomal translocation analysis from bronchial lavage indicates that such testing may serve as a useful diagnostic adjunct in MALT lymphoma with lung involvement.

Fibrosing interstitial lung diseases (FILDs), e.g., due to idiopathic pulmonary fibrosis (IPF), are chronic progressive diseases with a poor prognosis. The management of these diseases is challenging and focuses mainly on the suppression of progression with anti-fibrotic drugs. Therefore, novel FILD treatments are needed. In recent years, cell-based therapy with various stem cells has been investigated for FILD, and the use of mesenchymal stem cells (MSCs) has been widely reported and clinical studies are also ongoing. Induced pluripotent stem cells (iPSCs) have also been reported to have an anti-fibrotic effect in FILD; however, these have not been as well studied as MSCs in terms of the mechanisms and side effects. While MSCs show a potent anti-fibrotic effect, the possibility of quality differences between donors and a stable supply in the case of donor shortage or reduced proliferative capacity after cell passaging needs to be considered. The application of iPSC-derived cells has the potential to overcome these problems and may lead to consistent quality of the cell product and stable product supply. This review provides an overview of iPSCs and FILD, followed by the current status of cell-based therapy for FILD, and then discusses the possibilities and perspectives of FILD therapy with iPSC-derived cells.

Abstract Marine microplastics are one of the global environmental issues. The present study examined whether rubber tips of artificial sports fields could be marine microplastics. We observed the migration of rubber tips from the artificial turf field to the surrounding ditch connected to sewer pipes and then examined the ingestion of rubber tips using the goldfish Carassius auratus. The rubber tips found in sediments in the ditch suggest that the rubber tips could be sent to the river and released into the ocean. The goldfish ingested rubber tips with or without fish feed, and rubber tips were found in the intestine. However, the fish discharged the rubber tips within 48 h after ingestion. These results indicate that ingestion of the rubber tips was not accidental but an active behavior. Therefore, artificial turf sports fields could be a source of marine microplastics and may cause hazardous effects on wild fishes through ingestion.

A GaN-on-diamond structure is the most promising candidate for improving the heat dissipation efficiency of GaN-based power devices. Room-temperature bonding of GaN and diamond is an efficient technique for fabricating this structure. However, it is extremely difficult to polish diamond to an average roughness (Ra) below 0.4 nm, especially for polycrystalline diamond. In this work, Room-temperature bonding of GaN and rough-surfaced diamond with a SiC layer was successfully achieved by a surface-activated bonding (SAB) method. The diamond surface’s initial Ra value was 0.768 nm, but after deposition of the SiC layer, the Ra decreased to 0.365 nm. The SiC layer formed at the as-bonded GaN/diamond interface was amorphous, with a thickness of about 7 nm. After annealing at 1000-°C, the amorphous SiC layer became polycrystalline, and its thickness increased to approximately 12 nm. These results indicate that the deposition of a SiC layer on diamond can efficiently lower the diamond surface’s roughness and thus facilitate room-temperature bonding.

Abstract Background We conducted a phase II study of carboplatin plus nab‐paclitaxel for the treatment of small cell lung cancer (SCLC) after the failure of a prior standard chemotherapy containing platinum, etoposide, irinotecan, and amrubicin if indicated. Patients with interstitial pneumonia complications were included in the study. Methods Patients received 100 mg/m2 of nab‐paclitaxel weekly (on days 1, 8, and 15) and an AUC 5 of carboplatin on day 1. The study treatment was repeated every 3 weeks until disease progression or the appearance of unacceptable toxicities. The primary endpoint was the objective response rate. Results A total of 21 patients were enrolled, all of whom were eligible for inclusion in the analysis. Twelve patients had pre‐existing interstitial pneumonia. The overall response rate was 19.0% (90% confidence interval [CI]: 6.8%–38.4%). The lower limit of the 90% CI for the response rate did not exceed the prespecified threshold value of 10%. Among the 12 patients with pre‐existing interstitial pneumonia, the response rate was 25%. The median progression‐free survival time was 2.5 months (95% CI: 1.5–3.4 months), and the median survival time was 5.1 months (95% CI: 2.1–8.1 months). Two patients developed interstitial lung disease; both of these patients had pre‐existing interstitial pneumonia. One of the patients died from interstitial lung disease. Conclusion Combination chemotherapy with carboplatin plus nab‐paclitaxel for recurrent SCLC had a modest activity, although the primary study endpoint was not met. Further investigation of this regimen for patients with recurrent SCLC and interstitial pneumonia is warranted.

A new technique of diamond and InGaP room temperature bonding in atmospheric air is reported. Diamond substrate cleaned with H2SO4/H2O2 mixture solution is bonded to InGaP exposed after removing the GaAs layer by the H2SO4/H2O2/H2O mixture solution. The bonding interface is free from interfacial voids and mechanical cracks. An atomic intermixing layer with a thickness of about 8 nm is formed at the bonding interface, which is composed of C, In, Ga, P, and O atoms. After annealing at 400 °C, no exfoliation occurred along the bonding interface. An increase of about 2 nm in the thickness of the atomic intermixing layer is observed, which plays a role in alleviating the thermal stress caused by the difference of the thermal expansion coefficient between diamond and InGaP. The bonding interface demonstrates high thermal stability to device fabrication processes. This bonding method has a large potential for bonding large diameter diamond and semiconductor materials.

Mucosal-associated invariant T (MAIT) cells, a blossoming member of the innate-like T cells, play a pivotal role in host defense through engaging the mucosal immunity. Although it has been suggested that MAIT cells are somehow implicated in the allergic airway inflammation mediated by group 2 innate lymphoid cells (ILC2s) such as asthma, the precise role(s) of MAIT cells in such inflammation has remained elusive. To explore the possible roles of MAIT cells in the inflammation, we examined whether MAIT cells suppressed the production of T helper (Th) 2 and inflammatory cytokines from ILC2s, and constrained the proliferation of ILC2s, both of which are prerequisite for airway inflammation. Given that laboratory mice are poor at MAIT cells, a novel mouse line rich in MAIT cells was used. We found that mice rich in MAIT cells showed alleviated airway inflammation as evidenced by reduced infiltration of the immune cells and hyperplasia in goblet cells in the lung concomitant with compromised production of Th2 and inflammatory cytokines, while wild type mice exhibited severe inflammation upon challenge with the fungal extracts. In vitro coculture experiments using purified ILC2s and MAIT cells unrevealed that cytokine-stimulated MAIT cells suppressed ILC2s to produce the cytokines as well as to proliferate most likely via production of IFN-γ. Furthermore, reconstitution of the allergic airway inflammation in the highly immunocompromised mice showed that ILC2-mediated inflammation was alleviated in mice that received MAIT cells along with ILC2s. We concluded that MAIT cells played a crucial role in suppressing the cytokine-producing capacity of ILC2s and ILC2 proliferation, that ultimately led to decrease in the allergic airway inflammation.The results open up a novel therapeutic horizon in ILC2-mediated inflammatory diseases by modulating MAIT cell activity.

Pulmonary fibrosis is a life-threatening disease that has been attributed to several causes. Specifically, vascular injury is thought to be involved in the pathogenesis of fibrosis. The effects of the antifibrotic drug pirfenidone on angiogenesis have not been fully elucidated. This study aimed to investigate the effects of pirfenidone in human lung fibroblast–endothelial cell co-culture network formation and to analyze the underlying molecular mechanisms. Human lung fibroblasts were co-cultured with human umbilical vein endothelial cells to establish a co-culture network cell sheet. The influence of pirfenidone was evaluated for protective effect on the endothelial network in cell sheets stimulated with transforming growth factor β (TGF-β). Results indicated that TGF-β disrupted the network formation. Pirfenidone and Y27632 (Rho-associated coiled-coil containing protein kinase [Rho-kinase or ROCK] inhibitor) protected against the TGF-β–induced endothelial network disruption. TGF-β activated Rho-kinase signaling in cells composing the co-culture cell sheet, whereas pirfenidone and Y27632 inhibited these effects. In conclusion, TGF-β–induced Rho-kinase activation and disrupted endothelial network formation. Pirfenidone suppressed TGF-β–induced Rho-kinase activity in cell sheets, thereby enabling vascular endothelial cells networks to be preserved in the cell sheets. These findings suggest that pirfenidone has potential vascular network–preserving effect via inhibiting Rho-kinase activity in vascular injury, which is a precursor to pulmonary fibrosis.

Three-dimensional distribution of arsenic (As) dopants at Σ3{111}, Σ9{221}, Σ9{114}, and Σ9{111}/{115} grain boundaries (GBs) in silicon (Si) is examined by correlative analytical methods using atom probe tomography (APT) combined with low-temperature focused ion beam (LT-FIB), scanning transmission electron microscopy, and ab initio calculations. Σ3{111} GBs, consisting of only 6-membered rings with small bond distortions, do not exhibit an apparent As segregation. Meanwhile, it is hypothesized that As atoms would segregate at 5-membered rings in the other GBs via anisotropic bond distortions spontaneously introduced so as to lower the donor level, as Jahn-Teller distortions. In addition, APT combined with LT-FIB suggests preferential As segregation around stretched $$\left\langle {1\overline 1 0} \right\rangle $$ bonds reconstructed in Σ9{114} and Σ9{111}/{115} GBs, that are inevitably introduced in the $$\left\langle {1\overline 1 0} \right\rangle $$ tilt GBs with the tilt angle larger than 70.5°. It is hypothesized that As atoms would form As dimers at stretched $$\left\langle {1\overline 1 0} \right\rangle $$ bonds and the adjacent $$\langle 111\rangle $$ bonds, due to the tendency of As with five valence electrons to form a three-coordinated configuration, which is efficiently attained by an As dimer of a long length. This work provides important insights into As segregation at GBs; it is mainly determined by electronic interactions depending on the characteristics of valence electrons of As atoms, as well as on local bond distortions at GBs, via anisotropic bond distortions and dimerization.

Introduction: Vascular endothelial cell disorders are closely related to cardiovascular disease (CVD) and pulmonary diseases. Abnormal lipid metabolism in the endothelium leads to changes in cell signalling, and the expression of genes related to immunity and inflammation. It is therefore important to investigate the pathophysiology of vascular endothelial disorders in terms of lipid metabolism, using a disease model of endothelium. Methods: Human induced pluripotent stem cell-derived endothelial cells (iECs) were cultured on a matrigel to form an iEC network. Lipids in the iEC network were investigated by matrix-assisted laser desorption/ionization (MALDI) time-of-flight (TOF) imaging mass spectrometry (IMS) analysis. Ion fragments obtained by mass spectrometry were analysed using an infusion method, involving precursor ion scanning with fragment ion. Results: The MALDI TOF IMS analysis revealed co-localized intensity of peaks at m/z 592.1 and 593.1 in the iEC network. Tandem mass spectrometry (MS/MS) analysis by MALDI-imaging, in conjunction with precursor ion scanning using an infusion method with lipid extracts, identified that these precursor ions were lysophosphatidylcholine (LPC) (22:5) and its isotype. Conclusion: The MALDI-imaging analysis showed that LPC (22:5) was abundant in an iEC network. As an in vitro test model for disease and potential therapy, present analysis methods using MALDI-imaging combined with, for example, mesenchymal stem cells (MSC) to a disease derived iEC network may be useful in revealing the changes in the amount and distribution of lipids under various stimuli.

This study explored expectations regarding aging among a diverse cohort of undergraduates in Japan. A concurrent mixed methods design was employed with online administration of the Expectations Regarding Aging scale (ERA-12), and open-format and demographic questions among 133 culturally diverse undergraduates in Tokyo. Independent samples t-tests, one-way analysis of variance (ANOVA), descriptive sta­tistics, and thematic analysis were used to explore the data. ERA-12 scores and physical and cognitive function subscale results revealed negative perceptions about the aging process, while scores on the mental health subscale were significantly higher and positive. No significant differences emerged based on gender or cultural background. Qualitative data anal­ysis revealed student awareness of lifestyle influences on health in later life, concerns about current health and risk factors, and potential to tran­scend negative physical changes by finding meaning in other aspects of life. Understanding expectations regarding aging among younger cohorts may inform gerontological education and public health promotion to sup­port a life course approach to healthy aging.

Idiopathic pulmonary fibrosis (IPF) is a representative disease that causes fibrosis of the lungs. Its pathogenesis is thought to be characterized by sustained injury to alveolar epithelial cells and the resultant abnormal tissue repair, but it has not been fully elucidated. IPF is currently difficult to cure and is known to follow a chronic progressive course, with the patient’s survival period estimated at about three years. The disease occasionally exacerbates acutely, leading to a fatal outcome. In recent years, it has become evident that lipid metabolism is involved in the fibrosis of lungs, and various reports have been made at the cellular level as well as at the organic level. The balance among eicosanoids, sphingolipids, and lipid composition has been reported to be involved in fibrosis, with particularly close attention being paid to a bioactive lipid “lysophosphatidic acid (LPA)” and its pathway. LPA signals are found in a wide variety of cells, including alveolar epithelial cells, vascular endothelial cells, and fibroblasts, and have been reported to intensify pulmonary fibrosis via LPA receptors. For instance, in alveolar epithelial cells, LPA signals reportedly induce mitochondrial dysfunction, leading to epithelial damage, or induce the transcription of profibrotic cytokines. Based on these mechanisms, LPA receptor inhibitors and the metabolic enzymes involved in LPA formation are now considered targets for developing novel means of IPF treatment. Advances in basic research on the relationships between fibrosis and lipid metabolism are opening the path to new therapies targeting lipid metabolism in the treatment of IPF.

Abstract StarD7 facilitates phosphatidylcholine (PC) transfer to mitochondria, and is essential for mitochondrial homeostasis. However, the molecular mechanism for PC transfer by protein remains poorly understood. Herein, we describe a putative novel transmembrane (TM) domain C-terminal to the mitochondria-targeting signal (MTS) sequence at the N-terminus of StarD7. The mature form of StarD7 is integrated and/or associated onto the outer leaflet of the outer mitochondrial membrane (OMM) in HEPA-1 and HepG2 cells. A truncated form of StarD7 lacking the TM domain is distributed in the inner space of the mitochondria, and cannot reverse mitochondrial abnormalities, such as complex formation and PC content, when re-expressed in StarD7-KO HEPA-1 cells. Re-expression of wild StarD7 can compensate these mitochondrial functions of StarD7-KO HEPA-1 cells. The precursor form of StarD7 is cleaved between Met76 and Ala77, and Ala77 and Ala78 in the TM domain to produce the mature form. These results suggest that StarD7 is anchored onto the OMM through its N-terminal TM domain, and the C-terminal START domain may extend into the cytoplasm and shuttle PC between the ER and OMM at the ER-mitochondria contact sites.

Abstract Background Intelectin-1 (ITLN-1) is secreted by intestinal goblet cells and detectable in blood. Its expression is increased in IL-13-overexpressing mouse airways. However, its expression and function in human airways is poorly understood. Methods Distal and proximal bronchial epithelial cells (BECs) were isolated from bronchoscopic brushings of disease control (D-CON), COPD, inhaled corticosteroid-treated asthma (ST-Asthma) and inhaled corticosteroid-naïve asthma (SN-Asthma) patients. ITLN-1 mRNA expression in freshly isolated BECs, primary cultured BECs with or without IL-13 and inhibition effects of mometasone furoate (MF) were investigated by quantitative real-time PCR (qPCR). Correlations between ITLN-1 mRNA and Type-2 related parameters (e.g. FeNO, IgE, iNOS, CCL26, periostin and DPP4 mRNA) were analyzed. ITLN-1 protein distribution in asthmatic airway tissue was assessed by immunohistochemistry. Bronchial alveolar lavage (BAL) and serum ITLN-1 protein were measured by ELISA. The effect of recombinant human (rh) ITLN-1 on stimulated production of CXCL10 and phospho(p)-STAT1 expression examined in lung fibroblasts. Results ITLN-1 mRNA was expressed in freshly isolated BECs and was correlated with Type-2 related parameters. ITLN-1 protein was increased in goblet cells in SN-Asthmatics and increased in SN-Asthmatic BAL fluid. There were no any differences in serum ITLN-1 concentration between ST and SN-Asthma. IL-13 enhanced ITLN-1 expression and inhibited by MF from BECs in vitro, while rhITLN-1 inhibited CXCL10 production and p-STAT1 expression in HFL-1 cells. Conclusion ITLN-1 is induced by IL-13 and expressed mainly in goblet cells in untreated asthma where its levels correlate with known Type-2 related parameters. Further, ITLN-1 inhibits Type-1 chemokine expression.

Background and aims In many countries, early detection and diagnosis of autism spectrum disorder is largely dependent on parents’ initial concern with early symptoms of autism spectrum disorder. Previous research on parental perceptions of the autism spectrum disorder diagnostic process indicates that parental satisfaction may be due to either the timing of the diagnostic notification or the provision of post-diagnostic support. The objective of this research is to study the diagnostic notification process and its impact on parents who are informed of their young child’s diagnosis before they notice a problem and whose child undergoes early intervention therapy. Methods Eighty parents of preschool children diagnosed and undergoing early intervention for autism were surveyed to examine their experience of the diagnostic disclosure process. Results Of 68 respondents, 39 (58.2%) approved of the timing of diagnostic notification, while 10 of 13 dissatisfied respondents indicated that the diagnosis was communicated too late. However, there was no correlation between a higher degree of parental satisfaction with the diagnostic notification process and earlier timing of notification. Conclusions Although it is preferable to communicate a diagnosis of childhood autism as soon as possible, findings suggest that a highly individualized approach, allowing a degree of latitude in the timing of notification, may be permissible, depending on the individual case and parental readiness to receive the diagnosis. Implications Findings have clinical implications related to the concept of optimality of diagnostic disclosure as related to the diagnostic notification process, though later notification tends to lead to more dissatisfaction.

We have demonstrated that it is possible to reproducibly quantify hydrogen concentration in the SiN layer of a SiO2/SiN/SiO2 (ONO) stack structure using ultraviolet laser-assisted atom probe tomography (APT). The concentration of hydrogen atoms detected using APT increased gradually during the analysis, which could be explained by the effect of hydrogen adsorption from residual gas in the vacuum chamber onto the specimen surface. The amount of adsorbed hydrogen in the SiN layer was estimated by analyzing another SiN layer with an extremely low hydrogen concentration (

The research discussed in this paper proposed a control method that imparts equivalent friction to electronic power steering (EPS) systems in order to improve the steering feel. In order to impart friction stably, the proposed method uses motor torque rather than mechanical elements to impart friction. First, the effect of friction on the steering system was considered theoretically using simple harmonic motion models, and it was demonstrated theoretically that steering responsiveness could be increased by imparting appropriate friction force to the steering system. Based on the results of this analysis, a target value for equivalent friction force to be imparted by means of EPS control system was formulated. A method of linear approximation of the friction force necessary to realize equivalent friction force based on this target value was proposed. The method was applied in an actual vehicle, and the EPS system configuration necessary for the desired effect to be obtained was examined. It was considered that a system configuration incorporating a steering torque sensor with high torsional rigidity would be necessary, and a control method for imparting equivalent friction force was proposed. Finally, the effectiveness of the proposed method was verified in simulations using a vehicle model and in tests involving an actual vehicle. The vehicle model simulations demonstrated that the application of the proposed method increased steering responsiveness. The vehicle tests verified that the proposed method made it possible to obtain a stable steering feel, and was also effective in improving steering feel.

In this paper, we focused on the fact that the ease of driving changed according to torsional rigidity of the electric power steering system for the purpose of the improvement in control performance of vehicle. First, the influence on transfer characteristics from a steering angle(steering wheel) to front wheel angle(front tires) by torsional rigidity was considered theoretically. As a result, it turned out that a front wheel angle was determined by not only a steering angle but also the influence of the dynamic state of vehicle, and it was shown that the influence of the dynamic state of vehicle can be shut by making steering torsional rigidity into high torsional rigidity. Next, the validity of a theoretical verification was confirmed through numerical simulation of steering correction at the time of a disturbance input. Finally, the lower limit value of torsional rigidity for practical use of a high torsional rigidity steering was determined.

Airway inflammation is accompanied by infiltration of inflammatory cells and an abnormal response of airway smooth muscle. These cells secrete chemokines and express the cell surface chemokine receptors that play an important role in the migration and degranulation of inflammatory cells. Omalizumab is a monoclonal antibody directed against immunoglobulin E, and its blocking of IgE signaling not only reduces inflammatory cell infiltration mediated by the Th2 immune response but also inhibits other immune responses. The chemokine CCL15 is influenced by omalizumab, and the source of CCL15 has been reported to be airway smooth muscle cells and basophils. CCL15 binds to its receptor CCR1, which has been reported to be expressed by various inflammatory cells and also by airway smooth muscle cells. Therefore, CCL15/CCR1 signaling could be a target for the treatment of asthma. We review the role of CCL15 in the pathogenesis of asthma and also discuss the influence of IgE-mediated immunomodulation via CCL15 and its receptor CCR1.