Relevant bibliographies by topics / Lungs Immunology

Academic literature on the topic 'Lungs Immunology'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Lungs Immunology"

1

Wilkes, D. S., K. M. Heidler, L. K. Bowen, W. M. Quinlan, N. A. Doyle, O. W. Cummings, and C. M. Doerschuk. "Allogeneic bronchoalveolar lavage cells induce the histology of acute lung allograft rejection, and deposition of IgG2a in recipient murine lungs." Journal of Immunology 155, no. 5 (September 1, 1995): 2775–83. http://dx.doi.org/10.4049/jimmunol.155.5.2775.

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Abstract The immunologic and histologic changes associated with lung allograft rejection are believed to result from the presentation of donor lung alloantigens to recipient lymphocytes resulting in up-regulated Th1 lymphocyte activity. The ability of allogeneic lung immune cells to induce the pathologic and immunologic changes associated with acute lung allograft rejection are unknown. The current study determined whether allogeneic (C57BL/6, I-a(b)) bronchoalveolar lavage (BAL) cells (> or = 97% macrophages), when instilled into the lungs of recipient BALB/c mice (I-a(d)), induced the histology and immunology associated with acute lung allograft rejection. BALB/c mice received BAL cells from either C57BL/6 mice (allogeneic instillate) or BALB/c mice (autologous instillate) or PBS (control) by nasal insufflation weekly for 4 wk. Allogeneic BAL cells resulted in a lymphocytic bronchitis and vasculitis analogous to grade 1 to 2 lung allograft rejection. The mice given allogeneic instillates had a greater percentage of lymphocytes in the BAL fluid than those given autologous instillates. After instillation of allogeneic BAL cells, the Th1 cytokines, IL-2 and IFN-gamma (IFN-gamma), were produced locally in greater quantities and more frequently than Th2 cytokine IL-10. IL-4, another Th2 cytokine, was not detected. The local production of IgG1 and IgG2a, which are dependent on IL-4 and IFN-gamma, respectively, were increased. However, only IgG2a was deposited in the perivascular and peribronchiolar tissues. These data show that installation of allogeneic BAL cells into the airways of recipient mice induced up-regulated Th1 lymphocyte activity and caused the histologic changes associated with lung allograft rejection.
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2

polikepahad, sumanth, Jad El-Daye, Arash Naghavi, Jonathan Miller, Preethi Gunaratne, and David Brian Corry. "Lung RNA profiling suggests an essential role for micro RNAs in regulating allergic lung disease (91.9)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S161. http://dx.doi.org/10.4049/jimmunol.178.supp.91.9.

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Abstract MicroRNAs (miRNAs) are small non-coding RNAs, which negatively regulate gene expression by translational inhibition of target mRNAs. In vertebrates, miRNAs are produced in most organs, including lungs. In the current study, we hypothesized that the expression of miRNAs would correlate inversely with expression of critically important target genes involved in the pathogenesis of allergic lung disease. After intranasal challenge of mice with a potent allergen derived from Aspergillus oryzae on alternating days for 2 weeks, lungs were isolated, high quality RNA was extracted and subjected to microarray analysis in comparison to naïve lungs obtained in parallel. In allergic lungs, ~ 30 known miRNAs were suppressed and ~100 were induced, including many new miRNA candidates uncovered through genome-wide predictions. Bioinformatics analysis revealed that miRNA 199a*, which was suppressed, and miR-144 which was induced in allergic lungs, are candidate regulators of STAT-6, GATA-3 and costimulatory factors, all of which are critical mediators of allergic lung disease. These studies suggest the existence of many new miRNAs and pivotal role for miRNA 199a* in controlling the expression of allergic lung disease.
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Kulkarni, Hrishikesh Satish, Fuyi Liao, Lina Ma, Xiaobo Wu, Daniel Kreisel, John P. Atkinson, and Andrew E. Gelman. "C3 expression by lung transplants reduces alloimmune-mediated injury." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 69.21. http://dx.doi.org/10.4049/jimmunol.202.supp.69.21.

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Abstract Allograft injury is a major risk factor for death in lung transplant recipients. Complement protein C3 is primarily synthesized in the liver. However, a recent study by our group has demonstrated that C3 present in pulmonary epithelial cells can be augmented to facilitate their own ability to withstand acute environmental stress. Here, we hypothesized that pulmonary C3 expression reduces the severity of allograft rejection. To address this question, C3−/−left lungs [on a C57BL/6 (B6) background] were orthotopically transplanted into wildtype (WT) fully MHC mismatched (CBA/J) recipients. The right lung, native to the recipient, served as an internal control. CBA/J lungs transplanted into C3−/− recipients, C3−/− lungs transplanted into C3−/− recipients and CBA/J lungs transplanted into WT B6 recipients were also employed as controls. One week after transplantation, recipients were euthanized and evaluated for C3 levels and graft injury. C3 protein in C3−/− recipients of WT B6 and CBA/J lungs was not detected in the peripheral circulation but was expressed within graft tissues suggesting locally expressed C3 is sequestered within the lung. Signs of graft tissue injury were only observed in allogeneic recipients. However, acute rejection severity was significantly higher in C3−/− allografts when compared to WT allografts. Additionally, C3−/− allografts had a distinct pattern of acute alveolar damage and increased cellularity not evident in WT allografts. Taken collectively, our data indicate that expression of C3 by lung allografts attenuates alloimmunedependent responses that are associated with reduced survival in humans.
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Barker, Kimberly A., Anukul T. Shenoy, Nicole Stauffer-Smith, Emad Isam Arafa, Carolina Lyon de Ana, Alex Barron, Fumiaki Aihara, et al. "Lung resident memory B cells are a common and functionally significant component of lung adaptive immunity." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 85.8. http://dx.doi.org/10.4049/jimmunol.204.supp.85.8.

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Abstract Resident memory B cells (BRM) in influenza-recovered mouse lungs were recently described, but whether other types of infections elicit these cells is unknown. The relevance of BRM in human lungs and to lung immune defenses also remains unexplored. Using flow cytometry and immunofluorescence, we found that respiratory pneumococcal exposures in mice elicited lung BRM without concurrent tertiary lymphoid structure formation. Additionally, flow cytometry analysis of normal human lung tissue showed that human lungs are enriched compared to human blood for B cells bearing a resident memory phenotype. These findings indicate that lung BRM are a common feature of antigen-experienced lungs. Multiple mouse models were used to address the contributions of B cell immunity to anti-pneumococcal lung defenses. Mice exposed to a low virulence pneumococcal strain 4 weeks previously were well-protected from a serotype-mismatched pneumococcal challenge. When previously exposed mice were depleted of circulating B cells (but not lung B cells) with anti-CD20 treatment before the challenge infection, there was no effect on the acquired lung immunity. However, a genetically engineered mouse strain allowed effective depletion of lung B cells bearing PD-L2 (a mouse memory B cell marker) from previously exposed mice, and doing so before the virulent pneumococcal challenge resulted in substantial defects in bacterial clearance compared to mice with lung B cells intact. These results provide the first direct evidence of a role for lung BRM in anti-bacterial lung immunity. Notably, this defense was pneumococcal serotype-independent, distinguishing it from the serotype-specific immunity elicited by current pneumococcal vaccines.
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Nishinakamura, R., R. Wiler, U. Dirksen, Y. Morikawa, K. Arai, A. Miyajima, S. Burdach, and R. Murray. "The pulmonary alveolar proteinosis in granulocyte macrophage colony-stimulating factor/interleukins 3/5 beta c receptor-deficient mice is reversed by bone marrow transplantation." Journal of Experimental Medicine 183, no. 6 (June 1, 1996): 2657–62. http://dx.doi.org/10.1084/jem.183.6.2657.

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Mice mutant for granulocyte macrophage colony-stimulating factor (GM-CSF) or the common receptor component (beta c) for GM-CSF, interleukin (IL)-3, and IL-5 exhibit a lung disorder similar to human pulmonary alveolar proteinosis, a rare disease with congenital, infantile, and adult forms. Bone marrow transplantation and hematopoietic reconstitution of beta c mutant mice with wild-type bone marrow reversed the established disease state in the lungs, defining this disease as hematopoietic in nature. It is likely that the disease involves alveolar macrophages, as donor myeloid cell engraftment into the lungs of mutant recipient mice correlated with reverting both the disease and an abnormal macrophage morphology seen in the lungs of affected animals. Recombination Activating Gene-2 mutant donor bone marrow, which lacks the potential to develop lymphocytes, reversed the pathology in the lungs to the same extent as whole bone marrow. These data establish that certain lung disorders, if of cell-autonomous hematopoietic origin, can be manipulated by bone marrow transplantation.
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Lund, Sean J., Kathryn A. Patras, Jacqueline M. Kimmey, Asami Yamamura, Gilberto Hernandez, Omar Lakhdari, Alyssa M. McCoy, Victor Nizet, and Lawrence S. Prince. "Polysaccharide capsule allows Group B Streptococcus to avoid killing in a newborn pneumonia model." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 117.30. http://dx.doi.org/10.4049/jimmunol.200.supp.117.30.

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Abstract Group B Streptococcus (Streptococcus agalactiae, GBS) causes severe infections in neonates. While not a common adult pathogen, GBS is the leading cause of congenital pneumonia. To determine the molecular mechanisms of neonatal susceptibility, we developed a murine GBS pneumonia model. Neonatal, juvenile, and adult C57BL/6 mice were inoculated intranasally with 2800 CFU/g of GBS (COH1). After 7 d, survival was 100 % in adults and juveniles, with 10 % of neonates dying within 3 d after infection. Histopathological assessments showed severe lung injury scores 24 h after infection, with adult and juvenile mice demonstrating resolution of injury at 3 d post infection and normal histology after 7 d. In contrast, neonatal lungs had persistent lung injury up to 7 d post infection. By FACS, GBS induced rapid neutrophil recruitment into adult lungs and increased CD11b expression on adult lung macrophages. In neonatal lungs, GBS neither increased neutrophil numbers nor altered macrophage marker expression. Confocal imaging showed GBS in adult lungs almost entirely localized to alveolar macrophage phagolysosomes. However in neonatal lungs, GBS was only rarely phagocytosed by macrophages. These data were consistent with GBS killing data, which showed complete GBS killing within 24 h in adult and juvenile mice, but persistent GBS viability within the lung for up to 3 d in neonates. Defective GBS killing in neonates appeared to require the GBS capsule. Neonatal mice were much more efficient in killing the ΔcpsD capsule mutant compared to wild type GBS. Adult mice showed equal killing of ΔcpsD or wild type GBS. Our data suggest that the GBS capsule prevents killing by the newborn lung innate immune system, leading to neonatal disease susceptibility.
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Park, Juwon, Christina Lee, and Michelle D. Tallquist. "PDGFRα ablation leads to alteration of ECM and immune cell composition in the lung." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 74.20. http://dx.doi.org/10.4049/jimmunol.204.supp.74.20.

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Abstract Fibroblasts are the major cells responsible for tissue homeostasis, repair, and remodeling. In particular, PDGFRα is expressed by mesenchymal progenitors in the lung that constitute the myofibroblast population which transiently express α-SMA during alveologenesis. In the fibrotic lungs, PDGFRα+ lineages can differentiate into subpopulation of myofibroblasts which regulate tissue repair and remodeling. Although the contribution of PDGFRα+lineage to lung development and fibrosis are particularly well-known, their roles in the lung parenchyma at baseline are less characterized. To explore how PDGFRα+ fibroblasts affect extracellular matrix in baseline lung, we used genetic ablation of PDGFRα+ fibroblasts using Pdgfrα-CreERT2-driven expression of diphtheria toxin A. Histologically, thin mesenchyme was observed in fibroblast-ablated adult lungs. A majority of PDGFRα+ lineages are Col1a1-GFP+ cells, but PDGFRα-ablated lungs showed a significant decrease in the number of PDGFRα lineage and Col1a1-GFP+ cells. In addition, decreased expressions of ECM genes, such as Col1a1, Col1a2, and fibronectin-1 were observed in PDGFRα-ablated lungs. These data indicated that PDGFRα+ cells are a major source of extracellular proteins and PDGFRα ablation leads to alteration of ECM homeostasis in the baseline lung. Flow cytometry analysis of the lung tissues revealed that PDGFRα ablation resulted in elevated numbers of leukocytes and neutrophils. However, fibroblast loss did not affect macrophage numbers. These data suggested that fewer PDGFRα+ cells or loss of ECM or both can affect the recruitment of immune cells in the lung. In summary, changes in ECM environment by PDGFRα ablation leads to altered immune cell composition in the lung.
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Lorenzo, Erica, Jacob Hopkins, Julie Lefebvre, and Laura Haynes. "Vaccination does not protect aged mice from influenza-induced lung inflammation (VAC9P.1062)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 145.2. http://dx.doi.org/10.4049/jimmunol.194.supp.145.2.

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Abstract Aging predisposes individuals to increased susceptibility to influenza infection and delays in viral clearance. Importantly, we show that age-related delays in viral clearance are correlated with lingering inflammation in the lungs of aged mice. This is critical since inflammation in the lungs is associated with an enhanced susceptibility to secondary bacterial infection, which is a significant sequela to flu infection and often causes death. Inflammation in young lungs following flu infection can be significantly reduced by prior flu immunity, such as that generated following vaccination with recombinant influenza nucleoprotein (rNP). This protection is characterized by reduced lung inflammation, reduced lung damage, reduced susceptibility to flu challenge and also correlates with increased levels of IL-10 and anti-NP antibodies. In contrast, vaccination of aged mice with rNP does not reduce lung inflammation and shows no protection from weight loss and no reduction in viral titers in the lungs following subsequent flu infection. Additionally, aged mice generate lower levels of NP-specific antibodies, which are absolutely critical for reducing lung inflammation. Consequently, unlike young mice, these NP vaccinated aged mice are not protected from death due to secondary bacterial infection. Thus, when considering a universal flu vaccine such as rNP, it is important to understand how efficacious it can be in highly susceptible populations such as the elderly.
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Chapoval, Svetlana P., Ann E. Kelly-Welch, Elizabeth Smith, and Achsah D. Keegan. "Complex role of STAT6 in allergic airway inflammation (39.11)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S27. http://dx.doi.org/10.4049/jimmunol.178.supp.39.11.

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Abstract STAT6 plays a critical role in Th2 cell differentiation and in allergic lung inflammation. Using a chimeric mouse model, we observed alternative lung pathology in STAT6 KO mice even when WT bone marrow or Th2 cells were provided. Thus, we hypothesized that STAT6 contributes to inflammation in a complex manner. To detail STAT6 function, WT and STAT6 KO mice were subjected to OVA priming and challenges. Broncho-alveolar lavage (BAL) cell composition, lung histology, and FACS analysis of digested lungs were assessed 48h after the last challenge. As expected, eosinophils composed a majority of BAL cells in WT mice and less than 2% in STAT6 KO mice. The OVA-induced inflammation in STAT6 KO lungs was composed mainly of macrophages with small fractions of neutrophils and lymphocytes. The OVA-treated WT lungs showed strong although divergent expression of F4/80, Mac-2, and CD11b molecules; this was significantly reduced in STAT6 KO mice. However, the numbers of dendritic cells, B cells, CD4+ and CD8+ T cells in the lungs of OVA-treated mice were unaffected by STAT6 deficiency. Interestingly, STAT6 KO mice showed enhanced basal airway reactivity to methacholine and numbers of Mac-2+ cells as compared to WT mice, suggesting that STAT6 deficiency altered lung homeostasis. Taken together, our studies demonstrate STAT6-dependent and –independent features of asthma phenotype which may impact treatments targeting STAT6. (AI38985)
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Singh, Ram Raj, and Isela Valera. "Plasmacytoid dendritic cells contribute to pro-inflammatory and pro-fibrotic milieu in lung fibrosis." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 182.76. http://dx.doi.org/10.4049/jimmunol.202.supp.182.76.

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Abstract Fibrosis, the end-result of tissue injury in a wide range of diseases, contributes to >40% of mortality in the US. Plasmacytoid dendritic cells (pDC) are reduced in the peripheral blood, but increase in the lungs and skin of patients with systemic sclerosis, a prototypic fibrotic disease (JCI Insight 2018). The frequency of pDCs in the lungs of patients correlated with the severity of lung disease and with levels of proteins implicated in inflammation and fibrosis. Importantly, depletion of pDCs ameliorated lung and skin fibrosis in the bleomycin-induced animal model. pDC depletion also altered the expression levels of proteins and genes implicated in chemotaxis, inflammation, and fibrosis in the lungs. To test if pDCs directly contribute to inflammatory/profibrotic milieu in fibrosis, we injected C57Bl/6 mice with bleomycin, harvested lungs, and analyzed lungs for proteins by Western blot, ELISA, and flow cytometry. CD36 that is implicated in platelet-collagen adhesion, oxidative stress and inflammation was increased on pDCs but not on mDCs, other myeloid cells, B cells and T cells in the lungs of bleomycin-injected mice as compared to control mice. TLR7 was also increased more on pDCs than on all other immune cells examined, whereas TLR2 was increased more on mDCs and other myeloid cells but not on pDCs and B cells. TGFβ-latent peptide was higher on all immune cells examined in the lungs of bleomycin-injected animals than in controls. Among chemokine receptors, CCR2, CCR3, CCR6, CCR9 and CXCR4 were higher on pDCs than other cells. In summary, pDCs elicit profibrotic milieu in the development of systemic fibrosis. These observations identify the increased trafficking of pDCs’ to the affected organs as a therapeutic target in fibrosis.
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Dissertations / Theses on the topic "Lungs Immunology"

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Lemaitre, Philippe. "Early role of IL-17 and calcineurin inhibitor-mediated Th2- and Th17-polarization of chronic trachea allograft rejection pathways." Doctoral thesis, Universite Libre de Bruxelles, 2014. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209243.

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Lung transplantation is the only therapeutic approach for patients presenting end-stage pulmonary failure. Despite progress made in organ preservation and immunosuppression, primary graft dysfunction and obliterative bronchiolitis still hamper short-term and long-term outcomes, respectively. Interleukin-17 recently emerged as a major actor in several immuno-inflammatory disorders. Clinical and experimental evidence also suggest the implication of interleukin-17 or type 17 CD4+ T cells in lung rejection. We therefore investigated the contribution of this cytokine to graft pathology in a murine model of tracheal transplantation that recapitulates pathological features of lung rejection including the development of obliterative airway disease.

We first demonstrated that interleukin-17 contributes to inflammatory lesions in the early phase post-transplantation. Interleukin-17 was found to be produced by &61543;&61540;+ T cells and CD4+ T cells infiltrating the graft and interleukin-17 neutralization significantly reduced the development of epithelial lesions together with inhibition of interleukin-6 and heat-shock-protein 70 gene transcription.

We then investigated the contribution of interleukin-17 to obliterative airway disease. Although interleukin-17 did not play a dominant role in absence of immunosuppression, it was found to contribute to airway pathology in animals receiving cyclosporin A. Under this treatment, we first observed dramatic changes in the composition of the lymphocyte populations infiltrating the graft: the numbers of CD8+ T cells producing interferon-&61543; and type 1 CD4+ T cells were dramatically decreased while the numbers of type 17, and also type 2 CD4+ T cells were unaffected. The pathological relevance of these findings was first demonstrated by the prolongation of graft survival afforded by the depletion of CD4+ T cells in cyclosporin A-treated animals. Furthermore, graft rejection was also delayed in mice genetically deficient in either interleukin-17 or interleukin-4, providing evidence that type 17 and type 2 CD4+ T cells actively contribute to graft rejection in cyclosporin A-treated recipients. On the other hand, parallel experiments in interferon-&61543;-deficient mice revealed that interferon-&
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished

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2

Vanderstocken, Gilles. "Caractérisation du rôle des nucléotides extracellulaires et du récepteur purinergique P2Y2 dans la physiopathologie des maladies pulmonaires inflammatoires." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209591.

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Amongst respiratory diseases, inflammatory lung diseases constitute a major part of public

health problem. As a consequence, investigating the immune mechanisms that contribute to

the pathogenesis of these diseases is essential to identify candidate targets for the

development of new therapeutic drugs. Furthermore, over the past 20 years, the growing awareness

that purinergic signalling events shape the immune and inflammatory responses to infection and

allergic reactions warranted the development of animal models to assess their importance in vivo in

acute lung injury and chronic airway diseases. The field of purinergic inflammation formulated the

unifying concept that ATP is released as a «danger signal» to induce inflammatory responses upon

binding purinergic receptors.

According to these elements, we began in 2007 to evaluate lung inflammation in mice deficient for

the P2Y2 purinergic receptor in TH2 and TH1 models. The most convincing evidence that the P2Y2

receptor is engaged during alarm situations comes from studies related to cystic fibrosis and asthma.

Indeed, chronic respiratory diseases are commonly associated with elevated airway ATP

concentrations, as reported in cystic fibrosis, but also in idiopathic pulmonary fibrosis and chronic

obstructive pulmonary disease (COPD) patients, and they are raised by allergens in asthmatic

patients.

First, we demonstrated a significant role of the P2Y2R in a TH2-ovalbumin(OVA)-induced asthma

model. We observed that eosinophil accumulation, a distinctive feature of lung allergic inflammation,

was defective in OVA-treated P2Y2-deficient mice compared with OVA-treated wild type animals.

Interestingly, the upregulation of VCAM-1 was lower on lung endothelial cells of OVA-treated P2Y2

knockout mice compared with OVA-treated wild type animals. Adhesion assays demonstrated that

the action of UTP on leukocyte adhesion through the regulation of endothelial VCAM-1 was

abolished in P2Y2-deficient lung endothelial cells. Additionally, the level of soluble VCAM-1, reported

as an inducer of eosinophil chemotaxis, was strongly reduced in the bronchoalveolar lavage fluid of

P2Y2-deficient mice.

Secondly, we studied the consequences of P2Y2R loss in lung inflammation initiated after pneumonia

virus of mice (PVM) infection in collaboration with the group of Pr. Daniel Desmecht (ULg). We

demonstrated here that P2Y2

-/-

mice display a severe increase in morbidity and mortality rate in

response to PVM. Lower survival of P2Y2

-/-

mice was not correlated with excessive inflammation

despite the higher level of neutrophil recruiters in their broncho-alveolar fluids. Interestingly, we

observed lower numbers of dendritic cells, CD4

+

T cells and CD8

+

T cells in P2Y2

-/-

mice compared to

P2Y2

+/+

infected lungs. Lower level of IL-12 and higher level of IL-6 in broncho-alveolar fluid support

an inhibition of Th1 response in P2Y2

-/-

mice. Quantification of DC recruiter expression revealed

comparable IP-10 and MIP-3&
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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3

Fallata, Ghaith Mohammed. "Association of gut luminal metabolites and allergic responses." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1515185113264117.

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Todd, Anthony. "The immunology of extrinsic allergic alveolitis : with reference to bird breeders' lung." Thesis, University of Newcastle Upon Tyne, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287418.

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Ramis, Cabrer Daniel 1993. "From chronic obstructive pulmonary disease to lung cancer : an immunologic approach." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/667310.

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Se ha establecido que un subconjunto de pacientes con cáncer debuta con infiltrados inmunes que se organizan en agregados en el nicho tumoral y sus alrededores. Estas estructuras linfoides se desarrollan en respuesta a estímulos inflamatorios a través de un proceso estrechamente regulado. Además de su valor pronóstico, las TLSs pueden representar una nueva vía para las estrategias terapéuticas, pero actualmente se encuentra en etapas iniciales. En contraste con el papel en la activación inmune de las TLSs, en ciertos tumores, su efecto puede apuntar hacia la progresión tumoral como consecuencia de las condiciones altamente inmunosupresoras mediadas por las células malignas presentes en el nicho tumoral. Los datos preliminares proporcionados por la siguiente investigación sugieren que los pacientes con cáncer de pulmón podrían presentar un perfil inmunitario diferencial respecto a estos mismos que además subyacen EPOC. Este hecho podría presentar un impacto potencial en el pronóstico y la terapia de estos pacientes. Por otra parte, resultados procedentes de la actual investigación también revelan que ciertos marcadores cruciales presentes en diferentes vías de señalización involucradas con el estrés oxidativo, la apoptosis y la autofagia podría sobre expresarse en respuesta a la administración de inmunomoduladores. Estos datos ponen de manifiesto el interés de mecanismos adicionales relacionados con la inmunidad que podrían ser manipulados para asistir a la inmunidad contra el cáncer.
It is well established that a subset of cancer patients debuts with immune infiltrates, which organize into aggregates in the tumor niche and its vicinity. These lymphoid structures develop in response to inflammatory stimuli through a tightly regulated process. Besides the prognostic value of TLSs, they also may represent a novel avenue for therapeutic strategies, but it is currently still in its early stages. In contrast with the immune activator role of TLSs, in certain cancers, its effect may point towards tumor progression as a consequence of highly tumor-mediated immunosuppressive conditions present in the tumor niche. Preliminary data provided by the current investigation suggests that a differential immune profile may be present between LC patients and LC patients underlying COPD. This fact could present a potential impact in the prognosis and therapy of these patients. Moreover, crucial markers targeting different signaling pathways involved with oxidative stress, apoptosis, and autophagy were found to be overexpressed in response to immunomodulators administration in the current thesis. These data puts into manifest the interest of additional immunity-related mechanisms that could be targeted in order to assist immunity against cancer.
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6

Larsson, Emelie Olivia. "Immune to brain communication in allergic lung inflammation." Thesis, University of Southampton, 2013. https://eprints.soton.ac.uk/355709/.

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Asthma, a chronic TH2-mediated inflammatory disease of the airways, is the most common form of allergy in the Western world, affecting 300 million people worldwide. Epidemiological studies have shown that asthma is associated with mood disorders, such as anxiety and depression, and numerous experiments have reported that asthma induces functional changes in neuronal fibres of the peripheral nervous system (PNS), which innervate the brain. It is unknown, however, how allergic lung inflammation impacts on the central nervous system (CNS). The ability for peripheral inflammation to impact on the brain, altering behaviour and neuronal activity in the CNS, is a well-recognised and physiological phenomenon, known as immune to brain communication, but has, until now, only focused on how innate pro-inflammatory and TH1, but not TH2, type immune responses impact on the brain. Critically, immunomodulatory therapeutics, which involve stimulation of an innate pro-inflammatory immune response, are currently being developed for the treatment of asthma, highlighting the importance of understanding the effect of allergic lung inflammation and its treatment on the brain. Consequently, using acute and chronic localised TH2 models of inflammation, we investigated how allergic lung inflammation impacted on the CNS and subsequently determined the secondary impact of immunomodulation with the Toll-like receptor 7 (TLR7) agonist resiquimod. Acute TH2 inflammation in the peritoneum and lung was found to communicate with the brain, via a vagal route of communication. Crucially, it led to a distinct pattern of neuronal activity, with no changes in sickness behaviour or CNS inflammation, changes widely different to those known to occur following systemic TH1 inflammation. At chronic stages of lung inflammation, changes in genes associated with synaptic plasticity in the brainstem and altered expression of the GABAB receptor and brain-derived neurotrophic factor in the hippocampus were observed, firstly providing a CNS-dependent biological explanation for airway hyperresponsiveness, a critical pathological symptom of asthma, and secondly offering a biological justification for the prevalence of mood disorders in asthmatic patients. Resiquimod treatment in allergic animals was associated with attenuated central inflammatory responses, as compared to treatment in healthy animals, encouraging and reassuring in terms of patient well-being and, critically, also insinuating that safety of therapeutics differs in diseased, as opposed to healthy individuals. The results in this thesis are some of the first to identify that physiological inflammatory diseases impact on the CNS, highlighting the importance of immune to brain communication on pathological and psychopathological symptoms of a disease, and additionally demonstrating how inflammatory conditions can modify the off-target effects of a drug. Not only do these results provide a foundation for the future of immune to brain communication research, namely understanding how physiological inflammatory diseases impact on the CNS, but also have the potential to be translational and emulated in a clinical setting.
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White, Anna-Marie. "The role of tumour necrosis factor α in lung inflammation." Thesis, University of Bath, 1996. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362198.

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Singh, Ravinder. "The role of Death Receptor 3 in allergic lung inflammation." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/56963/.

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Death Receptor 3 (DR3) is a death domain containing member of the TNF Receptor Superfamily (TNFRSF), refereeing a range of cellular responses from differentiation and proliferation to cell death, depending upon the context of receptor activation. DR3 has been reported to have a role in many inflammatory diseases, including inflammatory arthritis and inflammatory bowel disease. The aim of this study was to determine the contribution of DR3 in a mouse model of acute and chronic allergic lung inflammation. Mice genetically deficient in the DR3 gene (DR3ko) were resistant to cellular accumulation within the lungs and bronchoalveolar lavage following acute lung inflammation, induced by priming with ovalbumin (OVA) and the adjuvant aluminium hydroxide (Alum) prior to 2 OVA aerosol exposures. To discern the role of DR3 in a more physiologically relevant chronic model of allergic lung inflammation, mice underwent repeated inhalation challenges with OVA subsequent to priming with OVA and Alum. Whilst cellular accumulation did not differ, DR3ko mice displayed reduced immuno-histopathology, and goblet cell hyperplasia, hallmarks of the asthmatic phenotype. Intriguingly, DR3ko mice exhibited reduced accumulation of various cell types into the spleen in both models. Early priming events were therefore investigated, prior to aerosolised antigenic challenge to decipher the effects of DR3. One sensitisation injection was sufficient to induce decreased DR3ko splenocyte accumulation, though T and B cell responses were observed to be comparable between DR3ko and DR3wt controls. DR3ko mice had depleted CXCL10 levels, suggesting cellular recruitment in response to inflammation is DR3 dependent. The underlying DR3 dependent mechanisms concerning the DR3ko splenic defects are under further investigation and may have impact on the use of the DR3/TL1A pathway as a therapeutic target, either as an anti-inflammatory or as a booster of the immune response to pathogens.
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Arko-Mensah, John. "Mycobacterial infection: Immune evasion, host susceptibility and immunological markers of diagnostic importance." Doctoral thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-8208.

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IIn the first study, we investigated the functional implications of prolonged TLR signalling on IFN-γ mediated killing of mycobacteria by murine macrophages in vitro. TLR2, but not TLR4 ligation interfered with IFN-γ mediated killing of mycobacteria in macrophages. In terms of mechanisms, neither TNF nor nitric oxide (NO) production was significantly affected, and the refractoriness induced could be reversed with increasing amounts of IFN-γ In the second study, we aimed to identify immunological markers of diagnostic importance in both the respiratory tract and serum during pulmonary mycobacterial infection in mice. We found that increased levels of immunological markers in the respiratory tract, but not serum, correlated better with active mycobacterial infection in the lungs, suggesting that the immune response in the respiratory tract is more reflective of the infection status and pathology than the systemic response. Finally, we investigated the level and nature of immune responses to pulmonary mycobacterial infection in BALB/c and C57BL/6 mice, two mouse strains known to exhibit different susceptibilities to infection with several intracellular pathogens, including mycobacteria. We showed that increased susceptibility of BALB/c mice to early mycobacterial infection was associated with reduced Th1 immune responses, and increased sTNFR secretion in the lung. Moreover, BALB/c mice recruited fewer monocytes/macrophages to the lung, and although IFN-γ stimulation of infected bone marrow derived macrophages in both mouse strains resulted in induction of antimycobacterial activity, BALB/c mice had a reduced capacity to kill ingested bacteria. The work presented in this thesis provide further insight into the mechanisms involved in the host-pathogen interaction; from persistence, to the immunological processes induced by the pathogen, to susceptibility of the host to infection.

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Hosker, Harold Stephen Ronald. "Alveolar macrophage and blood monocyte function in small cell lung cancer." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241364.

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Books on the topic "Lungs Immunology"

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1929-, Staub Norman C., ed. The Pulmonary intravascular macrophage. Mount Kisco, NY: Futura Pub. Co., 1989.

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A, Stockley Robert, ed. Pulmonary defences. Chichester: J. Wiley, 1997.

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Shennib, Hani. Immunology of the lung allograft. New York: Springer-Verlag, 1995.

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L, Kradin Richard, and Robinson Bruce W. S, eds. Immunopathology of lung disease. Boston: Butterworth-Heinemann, 1996.

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L, Rose Marlene, and Yacoub Magdi, eds. Immunology of heart and lung transplantation. London: Edward Arnold, 1993.

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1941-, Lipscomb Mary F., and Russell S. W, eds. Lung macrophages and dendritic cells in health and disease. New York: M. Dekker, 1997.

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1946-, Barnes Peter J., and Stockley Robert A, eds. Molecular biology of lung disease. Oxford: Blackwell Scientific Publications, 1994.

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Herman, Chmel, Bendinelli Mauro, and Friedman Herman 1931-, eds. Pulmonary infections and immunity. New York: Plenum Press, 1994.

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Williams, Marc A. Allergens and respiratory pollutants: The role of innate immunity. Oxford: Biohealthcare, 2011.

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Philip, Witorsch, and Spagnolo Samuel V, eds. Air pollution and lung disease in adults. Boca Raton, Fla: CRC Press, 1994.

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Book chapters on the topic "Lungs Immunology"

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Kurup, Viswanath P., and Alan P. Knutsen. "Fungal Hypersensitivity in the Lungs." In Fungal Immunology, 241–64. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-25445-5_12.

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Garvy, Beth A., and Francis Gigliotti. "Antibody-Mediated Immunity to Pneumocystis in the Lungs." In Fungal Immunology, 291–302. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-25445-5_14.

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Kawakami, Kazuyoshi. "Innate Immunity in the Lungs to Cryptococcal Infection." In Fungal Immunology, 135–55. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-25445-5_7.

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Feldmesser, Marta, and Arturo Casadevall. "Antibody-Mediated Immunity to Fungi in the Lungs." In Fungal Immunology, 181–200. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-25445-5_9.

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Romani, Luigina, and Paolo Puccetti. "Immune Regulation and Tolerance to Fungi in the Lungs and Skin." In Chemical Immunology and Allergy, 124–37. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000154957.

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Gimferrer, Idoia, and Karen A. Nelson. "Immunology in Lung Transplantation." In Lung Transplantation, 139–60. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91184-7_9.

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Zumla, Alimuddin, Sarah Rowland-Jones, and Andrew McMichael. "Lung Immunology and HIV." In AIDS and Respiratory Medicine, 15–40. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-3446-8_2.

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Dorn, Joshua M., Tamara C. Pozos, and Roshini S. Abraham. "Lung Abscess." In Pediatric Immunology, 339–41. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-21262-9_66.

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Gamondès, Delphine, and Didier Revel. "Immunologic Lung Disease." In Integrated Cardiothoracic Imaging with MDCT, 197–202. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-72387-5_12.

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Boghossian, Shahe. "Immunotherapy of Lung Tumors." In Cancer Immunology, 363–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46410-6_19.

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Conference papers on the topic "Lungs Immunology"

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Halvorsen, Elizabeth C., S. Elizabeth Franks, Brennan J. Wadsworth, Bryant T. Harbourne, Rachel A. Cederberg, Catherine A. Steer, Itziar Martinez-Gonzalez, Jack Calder, William W. Lockwood, and Kevin L. Bennewith. "Abstract A50: Interleukin-33 increases ST2+ regulatory T cells and promotes metastatic tumor growth in the lungs in an amphiregulin-dependent manner." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a50.

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Wang, Lei, Charlotte E. Pelgrim, Lucía N. Peralta Marzal, Stephanie Korver, Ingrid Van Ark, Thea Leusink-Muis, Ardy Van Helvoort, et al. "Mucosal immunology of the gut and lung in a cigarette smoke-induced murine model for COPD: the lung-gut axis." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.53.

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Roncaglioni, M. C., A. Falanga, A. P. Bolognese Dalessandro, B. Casali, and M. B. Donti. "ENZYMATIC AND IMMUNOLOGIC CHARACTERIZATION OF A CYSTEINE PROTEINASE PROCOAGULANT IN SEVERAL MURINE METASTASIZING TUMO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643663.

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Involvement of the hemostatic systemin tumor metastasis growth has been repeatedly suggested and several tumor-associated procoagulants have been described. We have studied here the procoagulant activity (PCA) of tissue extracts from 4 murine metastasizing tumors: Lewis Lung Carcinoma (3LL), B16 melanoma (B16), JW sarcoma (JWS) and the M4 variant of the mFS6 fibrosarcoma (M4). The experiments were designed to identify cancer procoagulant (CP) a FVII independent FX activating cysteine proteinase or tissue factor (TF) in these tumors. Tissue extracts from 3LL, B16 and JWS initiated coagulation both in the presence and absence of FVII (FVII independent activity ranging from 70% to 86% of the total activity). The PCA of the same tumors was significantly decreased (p < 0.01) by cysteine proteinase inhibitors (1 mM iodoacetamide (IA) and 0.1 mM HgCl2 ) and the inhibitionby HgCl2 was reversed by -SH group activators (di-thiatreital, KCN, IiDTA). In addition these samples were able of directly activating pure bovineFX in a two stage clotting assay. The PCA of M4 extract was dependent on FVII,was not significantly affected by IA and HgCl2 and was inhibited by concanavalin A, a known TF inhibitor. An Ouchterlony double immunodiffusion study showed immunological cross-reactivity of 3LL, B16 and JWS to a polyclonal antibody to purified CP (from rabbit V2 carcinoma; obtained from S.G. Gordon, Denver, USA). No cross-reactivity was present between this antibody and M4. This study shows that the PCA of M4 is TF, whereas the procoagulant(s) of 3LL, B16 and JWS are enzymatically and immunologically indistinguishable from CP.
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Schmidt, Leah M., Oanh Tran, Shannon Oda, Quintin Inman, Sasha Tan, Cody Jenkins, and Philip Greenberg. "Abstract PO079: Effects of the lung tumor microenvironment on T cell therapy." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po079.

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Maestre, Danay, Ryan D. Huff, Carley Schwartz, Anette K. Bølling, and Christopher Carlsten. "Di-butyl phthalate (DBP) augments allergen-induced lung function decline and alters lower airway innate immunology in crossover human study." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa1992.

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Carlsten, C., D. Maestre-Batlle, R. D. Huff, C. Schwartz, and A. K. Bølling. "Di-butyl Phthalate (DBP) Worsens Allergen-Induced Lung Function Decline and Alters Lower Airway Innate Immunology in Crossover Human Study." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1163.

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Hung, Jung-Jyh. "Abstract PO061: Prognostic significance of S100A2 expression in patients with resected lung adenocarcinoma." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po061.

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Lau, Denise, Michelle Stein, Jason Perera, Madhavi Kannan, and Aly Khan. "Abstract PR12: Genomic landscape of immunotherapy resistance in lung cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-pr12.

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Zhao, Chen, Weizhe Li, Chengcheng Jin, and Ronald N. Germain. "Abstract A62: Directly visualizing interactions between lung microbiota, tissue-resident immune cells and tumor cells in a genetically engineered lung adenocarcinoma mouse model." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a62.

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Jin, Chengcheng, Chen Zhao, Georgia Lagoudas, Arjun Bhutkar, Bo Hu, and Tyler Jacks. "Abstract A63: Commensal microbiota promote lung tumorigenesis via γδ T cells." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a63.

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