Publications
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Armstrong-James DPH, Bercusson A, Colley T, et al., 2018, Ibrutinib blocks Btk-dependent NF-ĸB and NFAT responses in human macrophages during Aspergillus fumigatus phagocytosis, Blood, Vol: 132, Pages: 1985-1988, ISSN: 1528-0020
Rhodes J, Argimon S, Chow NA, et al., 2018, Genomic epidemiology of Candida auris within the United Kingdom, and the future of whole genome sequencing typing, Publisher: OXFORD UNIV PRESS, Pages: S28-S28, ISSN: 1369-3786
Abdolrasouli A, Rhodes JL, Sewell TR, et al., 2018, Occurrence of triazole resistance in Aspergillus fumigatus among respiratory patients in a specialized cardio-thoracic centre, London, United Kingdom, Publisher: OXFORD UNIV PRESS, Pages: S76-S76, ISSN: 1369-3786
Rhodes J, Abdolrasouli A, Farrer RA, et al., 2018, Genomic epidemiology of the UK outbreak of the emerging human fungal pathogen Candida auris (vol 7, pg 43, 2018), EMERGING MICROBES & INFECTIONS, Vol: 7, ISSN: 2222-1751
Eades CP, Armstrong-James DPH, Periselneris J, et al., 2018, Improvement in Exophiala dermatitidis airway persistence and respiratory decline in response to interferon-gamma therapy in a patient with cystic fibrosis, Journal of Cystic Fibrosis, Vol: 17, Pages: e32-e34, ISSN: 1569-1993
Colley T, Sehra G, Chowdhary A, et al., 2018, In vitro and in vivo efficacy of a novel and long acting fungicidal azole, PC1244 on Aspergillus fumigatus infection, Antimicrobial Agents and Chemotherapy, Vol: 62, ISSN: 0066-4804
The antifungal effects of the novel triazole, PC1244, designed for topical or inhaled administration, againstA. fumigatushave been tested in a range ofin vitroandin vivostudies. PC1244 demonstrated potent antifungal activities against clinicalA. fumigatusisolates (N=96) with a MIC range of 0.016--0.25 μg/ml, whereas the MIC range for voriconazole was 0.25--0.5 μg/ml. PC1244 was a strong tight-binding inhibitor of recombinantA. fumigatusCYP51A and CYP51B (sterol 14α-demethylase) enzymes and strongly inhibited ergosterol synthesis inA. fumigatuswith an IC50of 8 nM. PC1244 was effective against a broad spectrum of pathogenic fungi (MIC ranged from <0.0078∼2 μg/ml), especially onAspergillus terreus,Trichophyton rubrum,Candida albicans,Candida glabrata,Candida krusei,Cryptococcus gattii,Cryptococcus neoformans and Rhizopus oryzaePC1244 also proved to be quickly absorbed into bothA. fumigatushyphae and bronchial epithelial cells, producing persistent antifungal effects. In addition, PC1244 showed fungicidal activity (MFC, 2 μg/ml), which was 8-fold more potent than voriconazole.In vivo, once daily intranasal administration of PC1244 (3.2 ∼ 80μg/mL) to temporarily neutropenic, immunocompromised mice 24h after inoculation with itraconazole-susceptibleA. fumigatussubstantially reduced fungal load in the lung, galactomannan in serum and circulating inflammatory cytokines. Furthermore, 7 days extended prophylaxis with PC1244 showed superiorin vivoeffects when compared against 1 day of prophylactic treatment, suggesting accumulation of the effects of PC1244. Thus, PC1244 has the potential to be a novel therapy for the treatment ofA. fumigatusinfection in the lungs of humans.
Rhodes JL, Abdolrasouli A, Farrer R, et al., 2018, Genomic epidemiology of the UK outbreak of the emerging human fungal pathogen Candida auris, Emerging Microbes and Infections, Vol: 7, ISSN: 2222-1751
Candida auris was first described in 2009, and has since caused nosocomial outbreaks, invasive infections and fungaemia across at least 19 countries in five continents. An outbreak of C. auris occurred in a specialised cardiothoracic London hospital between April 2015 and November 2016, which to date has been the largest outbreak within the UK, involving a total of 72 patients. To understand the genetic epidemiology of C. auris infection, both within this hospital and within a global context, we sequenced the outbreak isolate genomes using Oxford Nanopore Technologies and Illumina to detect antifungal resistance alleles and to reannotate the C. auris genome. Phylogenomic analysis placed the UK outbreak in the India/Pakistan clade, demonstrating an Asian origin: the outbreak showed similar genetic diversity to that of the entire clade and limited local spatiotemporal clustering was observed. One isolate displayed resistance to both echinocandins and 5-flucytosine; the former was associated with a serine to tyrosine amino acid substitution in the gene FKS1, and the latter was associated with a phenylalanine to isoleucine substitution in the gene FUR1. These mutations add to a growing body of research on multiple antifungal drug targets in this organism. Multiple differential episodic selection of antifungal resistant genotypes has occurred within a genetically heterogenous population across this outbreak, creating a resilient pathogen and making it difficult to define local-scale patterns of transmission as well as implementing outbreak control measures.
Rhodes J, Abdolrasouli A, Farrer R, et al., 2018, Rapid genome sequencing for outbreak analysis of the emerging human fungal pathogen Candida auris, Emerging Microbes and Infections, Vol: 7, ISSN: 2222-1751
Candida auris was first described in 2009, and it has since caused nosocomial outbreaks, invasive infections, and fungaemia across at least 19 countries on five continents. An outbreak of C. auris occurred in a specialized cardiothoracic London hospital between April 2015 and November 2016, which to date has been the largest outbreak in the UK, involving a total of 72 patients. To understand the genetic epidemiology of C. auris infection both within this hospital and within a global context, we sequenced the outbreak isolate genomes using Oxford Nanopore Technologies and Illumina platforms to detect antifungal resistance alleles and reannotate the C. auris genome. Phylogenomic analysis placed the UK outbreak in the India/Pakistan clade, demonstrating an Asian origin; the outbreak showed similar genetic diversity to that of the entire clade, and limited local spatiotemporal clustering was observed. One isolate displayed resistance to both echinocandins and 5-flucytosine; the former was associated with a serine to tyrosine amino acid substitution in the gene FKS1, and the latter was associated with a phenylalanine to isoleucine substitution in the gene FUR1. These mutations add to a growing body of research on multiple antifungal drug targets in this organism. Multiple differential episodic selection of antifungal resistant genotypes has occurred within a genetically heterogenous population across this outbreak, creating a resilient pathogen and making it difficult to define local-scale patterns of transmission and implement outbreak control measures.
Wrench C, Belchamber K, Bercusson A, et al., 2018, Reduced Clearance of Fungal Spores by Chronic Obstructive Pulmonary Disease GM-CSF- and M-CSF-derived Macrophages, Publisher: American Thoracic Society, Pages: 271-273, ISSN: 1044-1549
Armstrong-James D, de Boer L, Bercusson A, et al., 2018, From phagocytosis to metaforosis: calcineurin's deadly role in innate processing of fungi, PLoS Pathogens, Vol: 14, Pages: e1006627-e1006627, ISSN: 1553-7366
Shah A, Abdolrasouli A, Schelenz S, et al., 2017, Latent class modelling for pulmonary aspergillosis diagnosis in lung transplant recipients, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A13-A14, ISSN: 0040-6376
Rationale Timely, accurate diagnosis of invasive aspergillosis (IA) is key to enable initiation of antifungal therapy in lung transplantation. Despite promising novel fungal biomarkers, the lack of a diagnostic gold-standard creates difficulty in determining utility.Objectives This study aimed to use latent class modelling of fungal diagnostics to classify lung transplant recipients (LTR) with IA in a large single centre.Methods Regression models were used to compare composite biomarker testing of bronchoalveolar lavage to clinical and EORTC-MSG guideline-based diagnosis of IA with mortality used as a surrogate primary outcome measure. Bootstrap analysis identified radiological features associated with IA. Bayesian latent class modelling was used to define IA.Measurements and Main Results A clinical diagnosis of fungal infection (P =<0.001) and composite biomarker positive Results (P =<0.001) had significantly increased 12 month mortality. There was poor correlation between clinical diagnosis, EORTC-based IA diagnosis and composite biomarker positivity. Tracheobronchitis was positively predictive of a clinical and composite biomarker positive diagnosis of IA (p=0.004;95% CI–1.79–21.28 and p=0.03;95% CI–0.85–15.62 respectively). Latent class modelling resulted in the formation of 3 groups: Class 1: likely fungal infection; Class 2: unlikely fungal infection; Class 3: unclassifiable. A. fumigatus PCR was positive in ∼90% of class 1 LTRs compared to only 1% in class 2. Analysis of mortality showed a trend towards significance comparing class 1 with class 2 (p=0.06;HR–4.7;95% CI(0.91–24)) (figure 1).
Loss O, Bertuzzi M, Yan Y, et al., 2017, Mutual independence of alkaline- and calcium-mediated signalling in <i>Aspergillus fumigatus</i> refutes the existence of a conserved druggable signalling nexus, MOLECULAR MICROBIOLOGY, Vol: 106, Pages: 861-875, ISSN: 0950-382X
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- Citations: 8
Abdolrasouli A, Armstrong-James D, Ryan L, et al., 2017, In vitro efficacy of disinfectants utilised for skin decolonisation and environmental decontamination during a hospital outbreak with Candida auris, Mycoses, Vol: 60, Pages: 758-763, ISSN: 0933-7407
Candida auris has caused nosocomial infections and transmissions within hospital settings. As little is known about the efficacy of skin and environmental decontamination products to kill C. auris, this study investigated the in vitro activity of chlorine, chlorhexidine, iodine povidone and vaporised hydrogen peroxide products against C. auris. H2O2 vapour showed 96.6%-100% effective killing of C. auris. All isolates were inhibited by chlorhexidine gluconate concentrations at 0.125%-1.5% and for iodinated povidone at 0.07%-1.25%. Other species of Candida were also killed at 1000 ppm chlorine except C. parapsilosis which failed to be killed at 3 minutes contact time. We conclude that chlorhexidine gluconate, iodinated povidone, chlorine and H2O2 vapour demonstrate effective killing activity against C. auris at concentrations used in clinical practice.
Bercusson A, De Boer L, Warris A, et al., 2017, CFTR REGULATES NORMAL MACROPHAGE RESPONSES TO <i>ASPERGILLUS FUMIGATUS</i>, Publisher: WILEY, Pages: S255-S255, ISSN: 8755-6863
Armstrong-James D, 2017, TREATMENT OF FUNGAL INFECTIONS IN CYSTIC FIBROSIS: CURRENT APPROACHES AND NEW HORIZONS, Publisher: WILEY, Pages: S161-S161, ISSN: 8755-6863
Armstrong-James D, Brown GD, Netea MG, et al., 2017, Immunotherapeutic approaches to treatment of fungal diseases, Lancet Infectious Diseases, Vol: 17, Pages: e393-e402, ISSN: 1473-3099
Fungal infections cause morbidity worldwide and are associated with an unacceptably high mortality despite the availability of antifungal drugs. The incidence of mycoses is rising because of the HIV pandemic and because immunomodulatory drugs are increasingly used to treat autoimmune diseases and cancer. New classes of antifungal drugs have only been partly successful in improving the prognosis for patients with fungal infection. Adjunctive host-directed therapy is therefore believed to be the only option to further improve patient outcomes. Recent advances in the understanding of complex interactions between fungi and host have led to the design and exploration of novel therapeutic strategies in cytokine therapy, vaccines, and cellular immunotherapy, each of which might become viable adjuncts to existing antifungal regimens. In this report, we discuss immunotherapeutic approaches-the rationale behind their design, the challenges in their use, and the progress that is so urgently needed to overcome the devastating effect of fungal diseases.
Amarsaikhan N, Sands EM, Shah A, et al., 2017, Caspofungin Increases Fungal Chitin and Eosinophil and γδ T Cell-Dependent Pathology in Invasive Aspergillosis., Journal of Immunology, Vol: 199, Pages: 624-632, ISSN: 1550-6606
The polysaccharide-rich fungal cell wall provides pathogen-specific targets for antifungal therapy and distinct molecular patterns that stimulate protective or detrimental host immunity. The echinocandin antifungal caspofungin inhibits synthesis of cell wall β-1,3-glucan and is used for prophylactic therapy in immune-suppressed individuals. However, breakthrough infections with fungal pathogen Aspergillus fumigatus are associated with caspofungin prophylaxis. In this study, we report in vitro and in vivo increases in fungal surface chitin in A. fumigatus induced by caspofungin that was associated with airway eosinophil recruitment in neutropenic mice with invasive pulmonary aspergillosis (IA). More importantly, caspofungin treatment of mice with IA resulted in a pattern of increased fungal burden and severity of disease that was reversed in eosinophil-deficient mice. Additionally, the eosinophil granule proteins major basic protein and eosinophil peroxidase were more frequently detected in the bronchoalveolar lavage fluid of lung transplant patients diagnosed with IA that received caspofungin therapy when compared with azole-treated patients. Eosinophil recruitment and inhibition of fungal clearance in caspofungin-treated mice with IA required RAG1 expression and γδ T cells. These results identify an eosinophil-mediated mechanism for paradoxical caspofungin activity and support the future investigation of the potential of eosinophil or fungal chitin-targeted inhibition in the treatment of IA.
Armstrong-James D, Bicanic T, Brown GD, et al., 2017, AIDS-Related Mycoses: Current Progress in the Field and Future Priorities, TRENDS IN MICROBIOLOGY, Vol: 25, Pages: 428-430, ISSN: 0966-842X
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- Citations: 11
Cutino-Moguel M-T, Eades C, Rezvani K, et al., 2017, Immunotherapy for infectious diseases in haematological immunocompromise., Br J Haematol, Vol: 177, Pages: 348-356
Opportunistic infections remain a major problem across a broad spectrum of immunocompromised haematological patient groups, with viruses, bacteria, fungi and protozoa all presenting significant challenges. Given the major difficulties in treating many of these infections with the currently available antimicrobial chemotherapeutic arsenal, and the rapid emergence of antimicrobial resistance amongst all of the microbial kingdoms, novel strategies that enable host control or elimination of infection are urgently required. Recently, major progress has been made in our understanding of host immunocompromise in the haematological patient. In addition, a wide range of novel immunomodulatory strategies for infectious diseases have been developed. Here we discuss the major and wide-ranging areas of progress that have been made for host-directed immunotherapies in the context of infectious diseases, with relevance to haematological immunocompromise.
Alsuliman A, Muftuoglu M, Khoder A, et al., 2017, A subset of virus-specific CD161(+) T cells selectively express the multidrug transporter MDR1 and are resistant to chemotherapy in AML., Blood, Vol: 129, Pages: 740-758
The establishment of long-lived pathogen-specific T cells is a fundamental property of the adaptive immune response. However, the mechanisms underlying long-term persistence of antigen-specific CD4(+) T cells are not well-defined. Here we identify a subset of memory CD4(+) T cells capable of effluxing cellular toxins, including rhodamine (Rho), through the multidrug efflux protein MDR1 (also known as P-glycoprotein and ABCB1). Drug-effluxing CD4(+) T cells were characterized as CD161(+)CD95(+)CD45RA(-)CD127(hi)CD28(+)CD25(int) cells with a distinct chemokine profile and a Th1-polarized pro-inflammatory phenotype. CD4(+)CD161(+)Rho-effluxing T cells proliferated vigorously in response to stimulation with anti-CD3/CD28 beads and gave rise to CD161(-) progeny in vitro. These cells were also capable of self-renewal and maintained their phenotypic and functional characteristics when cultured with homeostatic cytokines. Multidrug-effluxing CD4(+)CD161(+) T cells were enriched within the viral-specific Th1 repertoire of healthy donors and patients with acute myeloid leukemia (AML) and survived exposure to daunorubicin chemotherapy in vitro. Multidrug-effluxing CD4(+)CD161(+) T cells also resisted chemotherapy-induced cytotoxicity in vivo and underwent significant expansion in AML patients rendered lymphopenic after chemotherapy, contributing to the repopulation of anti-CMV immunity. Finally, after influenza vaccination, the proportion of influenza-specific CD4(+) T cells coexpressing CD161 was significantly higher after 2 years compared with 4 weeks after immunization, suggesting CD161 is a marker for long-lived antigen-specific memory T cells. These findings suggest that CD4(+)CD161(+) T cells with rapid efflux capacity contribute to the maintenance of viral-specific memory T cells. These data provide novel insights into mechanisms that preserve antiviral immunity in patients undergoing chemotherapy and have implications for the development of novel immunotherapeutic appr
Schelenz S, Hagen F, Rhodes JL, et al., 2016, First hospital outbreak of the globally emerging Candida auris in a European hospital, Antimicrobial Resistance and Infection Control, Vol: 5, ISSN: 2047-2994
Background: Candida auris is a globally emerging multidrug resistant fungal pathogen causing nosocomial transmission.We report an ongoing outbreak of C. auris in a London cardio-thoracic center between April 2015 and July 2016. This isthe first report of C. auris in Europe and the largest outbreak so far. We describe the identification, investigation andimplementation of control measures.Methods: Data on C. auris case demographics, environmental screening, implementation of infection prevention/controlmeasures, and antifungal susceptibility of patient isolates were prospectively recorded then analysed retrospectively.Speciation of C. auris was performed by MALDI-TOF and typing of outbreak isolates performed by amplified fragmentlength polymorphism (AFLP).Results: This report describes an ongoing outbreak of 50 C. auris cases over the first 16 month (April 2015 to July 2016)within a single Hospital Trust in London. A total of 44 % (n = 22/50) patients developed possible or proven C. aurisinfection with a candidaemia rate of 18 % (n = 9/50). Environmental sampling showed persistent presence of the yeastaround bed space areas. Implementation of strict infection and prevention control measures included: isolationof cases and their contacts, wearing of personal protective clothing by health care workers, screening ofpatients on affected wards, skin decontamination with chlorhexidine, environmental cleaning with chorinebased reagents and hydrogen peroxide vapour. Genotyping with AFLP demonstrated that C. auris isolates fromthe same geographic region clustered.Conclusion: This ongoing outbreak with genotypically closely related C. auris highlights the importance ofappropriate species identification and rapid detection of cases in order to contain hospital acquired transmission.
Shah A, Armstrong-James D, 2016, Opportunist Turns Allergen: Double Life of Pneumocystis jirovecii in Asthma., American Journal of Respiratory and Critical Care Medicine, Vol: 194, Pages: 779-780, ISSN: 1535-4970
Bercusson A, de Boer L, Armstrong-James D, 2016, Endosomal sensing of fungi: current understanding and emerging concepts, Medical Mycology, ISSN: 1460-2709
Endosomal sensing represents a key strategy by which mammalian cells detect parasitization by invading pathogens. This is critical for the control of fungal pathogens, which are for the most part phagocytosed by effector cells of the innate immune system. Despite rapid overall progress in our understanding of endosomal responses in recent times, relatively little is known about how the endosomal sensing system detects fungi and the ensuing immunological consequences. Considering that many fungal pathogens must overcome and evade endosomal killing in order to survive in the host, understanding this key area of the early innate response is crucial for our understanding of fungal infection. In this review we present a summary of our current knowledge of endosomal sensing within the context of fungal pathogens, with a focus on the myeloid compartment.
Sekine T, Marin D, Cao K, et al., 2016, Specific combinations of donor and recipient KIR-HLA genotypes predict for large differences in outcome after cord blood transplantation, Blood, Vol: 128, Pages: 297-312, ISSN: 0006-4971
The ability of cord blood transplantation (CBT) to prevent relapse depends partly on donor natural killer (NK) cell alloreactivity. NK effector function depends on specific killer-cell immunoglobulin-like receptors (KIR) and HLA interactions. Thus, it is important to identify optimal combinations of KIR-HLA genotypes in donors and recipients that could improve CBT outcome. We studied clinical data, KIR and HLA genotypes, and NK-cell reconstitution in CBT patients (n = 110). Results were validated in an independent cohort (n = 94). HLA-KIR genotyping of recipient germline and transplanted cord blood (CB) grafts predicted for large differences in outcome. Patients homozygous for HLA-C2 group alleles had higher 1-year relapse rate and worse survival after CBT than did HLA-C1/C1 or HLA-C1/C2 (HLA-C1/x) patients: 67.8% vs 26.0% and 15.0% vs 52.9%, respectively. This inferior outcome was associated with delayed posttransplant recovery of NK cells expressing the HLA-C2-specific KIR2DL1/S1 receptors. HLA-C1/x patients receiving a CB graft with the combined HLA-C1-KIR2DL2/L3/S2 genotype had lower 1-year relapse rate (6.7% vs 40.1%) and superior survival (74.2% vs 41.3%) compared with recipients of grafts lacking KIR2DS2 or HLA-C1. HLA-C2/C2 patients had lower relapse rate (44.7% vs 93.4%) and better survival (30.1% vs 0%) if they received a graft with the combined HLA-C2-KIR2DL1/S1 genotype. Relapsed/refractory disease at CBT, recipient HLA-C2/C2 genotype, and donor HLA-KIR genotype were independent predictors of outcome. Thus, we propose the inclusion of KIR genotyping in graft selection criteria for CBT. HLA-C1/x patients should receive an HLA-C1-KIR2DL2/L3/S2 CB graft, while HLA-C2/C2 patients may benefit from an HLA-C2-KIR2DL1/S1 graft.
Adlakha A, Armstrong-James DPH, Lenhard B, 2016, The role of calcineurin inhibition in the dendritic cell response to Aspergillus fumigatus infection in lung transplant recipients, Publisher: LIPPINCOTT WILLIAMS & WILKINS, Pages: S371-S371, ISSN: 0041-1337
Armstrong-James DPH, 2016, Calcineurin Orchestrates Lateral Transfer of Aspergillus fumigatus during Macrophage Cell Death, American Journal of Respiratory and Critical Care Medicine, Vol: 194, Pages: 1127-1139, ISSN: 1535-4970
Rationale: Pulmonary aspergillosis is a lethal mold infection in the immunocompromised host. Understanding initial control of infection and how this is altered in the immunocompromised host are key goals for comprehension of the pathogenesis of pulmonary aspergillosis.Objectives: To characterize the outcome of human macrophage infection with Aspergillus fumigatus and how this is altered in transplant recipients on calcineurin inhibitor immunosuppressants.Methods: We defined the outcome of human macrophage infection with A. fumigatus, as well as the impact of calcineurin inhibitors, through a combination of single-cell fluorescence imaging, transcriptomics, proteomics, and in vivo studies.Measurements and Main Results: Macrophage phagocytosis of A. fumigatus enabled control of 90% of fungal germination. However, fungal germination in the late phagosome led to macrophage necrosis. During programmed necroptosis, we observed frequent cell–cell transfer of A. fumigatus between macrophages, which assists subsequent control of germination in recipient macrophages. Lateral transfer occurred through actin-dependent exocytosis of the late endosome in a vasodilator-stimulated phosphoprotein envelope. Its relevance to the control of fungal germination was also shown by direct visualization in our zebrafish aspergillosis model in vivo. The calcineurin inhibitor FK506 (tacrolimus) reduced cell death and lateral transfer in vitro by 50%. This resulted in uncontrolled fungal germination in macrophages and also resulted in hyphal escape.Conclusions: These observations identify programmed, necrosis-dependent lateral transfer of A. fumigatus between macrophages as an important host strategy for controlling fungal germination. This process is critically dependent on calcineurin. Our studies provide fundamental insights into the pathogenesis of pulmonary aspergillosis in the immunocompromised host.
Adlakha A, Armstrong-James D, Lenhard B, 2016, Effect of calcineurin inhibition on phenotypic maturation of dendritic cells in an in-vitro model of invasive aspergillosis in lung transplant recipients, Spring Meeting on Clinician Scientists in Training, Publisher: ELSEVIER SCIENCE INC, Pages: 16-16, ISSN: 0140-6736
Belchamber KBR, Shah A, Barnes PJ, et al., 2016, Defective Phagocytosis Of Aspergillus Fumigatus By COPD Macrophages, International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Shah A, Kannambath S, Herbst S, et al., 2015, 'THE KISS OF DEATH' - CALCINEURIN INHIBITORS PREVENT ACTIN-DEPENDENT LATERAL TRANSFER OF ASPERGILLUS FUMIGATUS IN NECROPTOTIC HUMAN MACROPHAGES, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A48-A48, ISSN: 0040-6376
Adlakha AG, Armstrong-James DPH, Lenhard B, 2015, CALCINEURIN INHIBITION IMPAIRS PHENOTYPIC MATURATION OF DENDRITIC CELLS IN A IN VITRO MODEL OF INVASIVE ASPERGILLOSIS IN LUNG TRANSPLANT RECIPIENTS, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A48-A49, ISSN: 0040-6376
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