Datasheet: MCA1928F Product Details

Total Page:16

File Type:pdf, Size:1020Kb

Datasheet: MCA1928F Product Details Datasheet: MCA1928F Description: RAT ANTI MOUSE CD153:FITC Specificity: CD153 Format: FITC Product Type: Monoclonal Antibody Clone: RM153 Isotype: IgG2b Quantity: 0.1 mg Product Details Applications This product has been reported to work in the following applications. This information is derived from testing within our laboratories, peer-reviewed publications or personal communications from the originators. Please refer to references indicated for further information. For general protocol recommendations, please visit www.bio-rad-antibodies.com/protocols. Yes No Not Determined Suggested Dilution Flow Cytometry Neat - 1/10 Where this antibody has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the antibody for use in their own system using appropriate negative/positive controls. Target Species Mouse Product Form Purified IgG conjugated to Fluorescein Isothiocyanate Isomer 1 (FITC) - liquid Max Ex/Em Fluorophore Excitation (nm) Emission (nm) FITC 490 520 Preparation Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant Buffer Solution Phosphate buffered saline Preservative 0.09% Sodium Azide Stabilisers 1% Bovine Serum Albumin Approx. Protein IgG concentration 0.1 mg/ml Concentrations Immunogen Mouse CD153/CHO cells. External Database Links UniProt: P32972 Related reagents Entrez Gene: Page 1 of 3 21949 Tnfsf8 Related reagents Synonyms Cd30l, Cd30lg Fusion Partners Spleen cells from immunized SD rats were fused with cells of the P3U1 mouse myeloma cell line. Specificity Rat anti Mouse CD153 antibody, clone RM153 recognizes murine CD153, also known as (CD30 ligand), a 40 kDa type II transmembrane protein belonging to the TNF superfamily. In the mouse CD153 is expressed primarily on activated CD4+ve T cells. The interaction of CD153 with its ligand CD30 is reported to enhance the proliferation of anti-CD3/CD28 co-stimulated T-cells. Clone RM153 is reported to block the functional binding of CD153 and can be used to inhibit the binding of murine CD30 to CD153 (Shimozato et al. 1999). Flow Cytometry Use 10ul of the suggested working dilution to label 106 cells in 100ul. The Fc region of monoclonal antibodies may bind non-specifically to cells expressing low affinity Fc receptors. This may be reduced by using SeroBlock FcR (BUF041A/B). References 1. Shimozato, O. et al. (1999) Expression of CD30 ligand (CD153) on murine activated T cells. Biochem Biophys Res Commun. 256 (3): 519-26. 2. Akiba, H. et al. (2000) Critical contribution of OX40 ligand to T helper cell type 2 differentiation in experimental leishmaniasis. J Exp Med. 191: 375-80. 3. Mori, M. et al. (1999) CD30-CD30 ligand interaction in primary cutaneous CD30(+) T-cell lymphomas: A clue to the pathophysiology of clinical regression. Blood. 94: 3077-83. Storage Store at +4oC or at -20oC if preferred. This product should be stored undiluted. Storage in frost free freezers is not recommended. This product is photosensitive and should be protected from light. Avoid repeated freezing and thawing as this may denature the antibody. Should this product contain a precipitate we recommend microcentrifugation before use. Shelf Life 18 months from date of despatch. Health And Safety Material Safety Datasheet Documentation #10041 available at: Information https://www.bio-rad-antibodies.com/uploads/MSDS/10041.pdf Regulatory For research purposes only Related Products Recommended Useful Reagents MOUSE SEROBLOCK FcR (BUF041A) MOUSE SEROBLOCK FcR (BUF041B) Page 2 of 3 North & South Tel: +1 800 265 7376 Worldwide Tel: +44 (0)1865 852 700 Europe Tel: +49 (0) 89 8090 95 21 America Fax: +1 919 878 3751 Fax: +44 (0)1865 852 739 Fax: +49 (0) 89 8090 95 50 Email: [email protected] Email: [email protected] Email: [email protected] 'M301325:170109' Printed on 26 Jun 2017 © 2017 Bio­Rad Laboratories Inc | Legal | Imprint Page 3 of 3.
Recommended publications
  • Critical Contribution of OX40 Ligand to T Helper Cell Type 2
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central Brief Definitive Report Critical Contribution of OX40 Ligand to T Helper Cell Type 2 Differentiation in Experimental Leishmaniasis By Hisaya Akiba,*§ Yasushi Miyahira,‡ Machiko Atsuta,*§ Kazuyoshi Takeda,*§ Chiyoko Nohara,* Toshiro Futagawa,* Hironori Matsuda,* Takashi Aoki,‡ Hideo Yagita,*§ and Ko Okumura*§ From the *Department of Immunology and the ‡Department of Parasitology, Juntendo University School of Medicine, Tokyo 113-8421, Japan; and §CREST (Core Research for Evolutional Science and Technology) of Japan Science and Technology Corporation, Tokyo 101-0062, Japan Abstract Infection of inbred mouse strains with Leishmania major is a well characterized model for analy- sis of T helper (Th)1 and Th2 cell development in vivo. In this study, to address the role of co- stimulatory molecules CD27, CD30, 4-1BB, and OX40, which belong to the tumor necrosis factor receptor superfamily, in the development of Th1 and Th2 cells in vivo, we administered monoclonal antibody (mAb) against their ligands, CD70, CD30 ligand (L), 4-1BBL, and OX40L, to mice infected with L. major. Whereas anti-CD70, anti-CD30L, and anti–4-1BBL mAb ex- hibited no effect in either susceptible BALB/c or resistant C57BL/6 mice, the administration of anti-OX40L mAb abrogated progressive disease in BALB/c mice. Flow cytometric analysis indicated that OX40 was expressed on CD41 T cells and OX40L was expressed on CD11c1 dendritic cells in the popliteal lymph nodes of L. major–infected BALB/c mice. In vitro stimu- lation of these CD41 T cells showed that anti-OX40L mAb treatment resulted in substantially reduced production of Th2 cytokines.
    [Show full text]
  • Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse
    Welcome to More Choice CD Marker Handbook For more information, please visit: Human bdbiosciences.com/eu/go/humancdmarkers Mouse bdbiosciences.com/eu/go/mousecdmarkers Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse CD3 CD3 CD (cluster of differentiation) molecules are cell surface markers T Cell CD4 CD4 useful for the identification and characterization of leukocytes. The CD CD8 CD8 nomenclature was developed and is maintained through the HLDA (Human Leukocyte Differentiation Antigens) workshop started in 1982. CD45R/B220 CD19 CD19 The goal is to provide standardization of monoclonal antibodies to B Cell CD20 CD22 (B cell activation marker) human antigens across laboratories. To characterize or “workshop” the antibodies, multiple laboratories carry out blind analyses of antibodies. These results independently validate antibody specificity. CD11c CD11c Dendritic Cell CD123 CD123 While the CD nomenclature has been developed for use with human antigens, it is applied to corresponding mouse antigens as well as antigens from other species. However, the mouse and other species NK Cell CD56 CD335 (NKp46) antibodies are not tested by HLDA. Human CD markers were reviewed by the HLDA. New CD markers Stem Cell/ CD34 CD34 were established at the HLDA9 meeting held in Barcelona in 2010. For Precursor hematopoetic stem cell only hematopoetic stem cell only additional information and CD markers please visit www.hcdm.org. Macrophage/ CD14 CD11b/ Mac-1 Monocyte CD33 Ly-71 (F4/80) CD66b Granulocyte CD66b Gr-1/Ly6G Ly6C CD41 CD41 CD61 (Integrin b3) CD61 Platelet CD9 CD62 CD62P (activated platelets) CD235a CD235a Erythrocyte Ter-119 CD146 MECA-32 CD106 CD146 Endothelial Cell CD31 CD62E (activated endothelial cells) Epithelial Cell CD236 CD326 (EPCAM1) For Research Use Only.
    [Show full text]
  • Uva-DARE (Digital Academic Repository)
    UvA-DARE (Digital Academic Repository) Balancing effector lymphocyte formation via CD27-CD70 interactions Arens, R. Publication date 2003 Link to publication Citation for published version (APA): Arens, R. (2003). Balancing effector lymphocyte formation via CD27-CD70 interactions. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl) Download date:27 Sep 2021 Chapter 3 Constitutive CD27/CD70 interaction induces expansion of effector-type T cells and results in IFNy-mediated B cell depletion Ramon Arens*, Kiki Tesselaar*, Paul A. Baars, Gijs M.W. van Schijndel, Jenny Hendriks, Steven T. Pals, Paul Krimpenfort, Jannie Borst, Marinus H.J. van Oers, and René A.W. van Lier 'These authors contributed equally to this work Immunity 15, 801-812 (2001) Chapter 3 Constitutive CD27/CD70 interaction induces expansion of effector-type T cells and results in IFNy-mediated B cell depletion Ramon Arens123#, Kiki Tesselaar23", Paul A.
    [Show full text]
  • Dendritic Cell Expression of CD70 in Vivo Potent Cellular Immunity By
    Combined TLR/CD40 Stimulation Mediates Potent Cellular Immunity by Regulating Dendritic Cell Expression of CD70 In Vivo This information is current as Phillip J. Sanchez, Jennifer A. McWilliams, Catherine of September 25, 2021. Haluszczak, Hideo Yagita and Ross M. Kedl J Immunol 2007; 178:1564-1572; ; doi: 10.4049/jimmunol.178.3.1564 http://www.jimmunol.org/content/178/3/1564 Downloaded from References This article cites 57 articles, 25 of which you can access for free at: http://www.jimmunol.org/content/178/3/1564.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 25, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Combined TLR/CD40 Stimulation Mediates Potent Cellular Immunity by Regulating Dendritic Cell Expression of CD70 In Vivo1 Phillip J. Sanchez,* Jennifer A. McWilliams,* Catherine Haluszczak,* Hideo Yagita,† and Ross M. Kedl2* We previously showed that immunization with a combination of TLR and CD40 agonists (combined TLR/CD40 agonist immu- nization) resulted in an expansion of Ag-specific CD8 T cells exponentially greater than the expansion observed to immunization with either agonist alone.
    [Show full text]
  • Gene Symbol Category ACAN ECM ADAM10 ECM Remodeling-Related ADAM11 ECM Remodeling-Related ADAM12 ECM Remodeling-Related ADAM15 E
    Supplementary Material (ESI) for Integrative Biology This journal is (c) The Royal Society of Chemistry 2010 Gene symbol Category ACAN ECM ADAM10 ECM remodeling-related ADAM11 ECM remodeling-related ADAM12 ECM remodeling-related ADAM15 ECM remodeling-related ADAM17 ECM remodeling-related ADAM18 ECM remodeling-related ADAM19 ECM remodeling-related ADAM2 ECM remodeling-related ADAM20 ECM remodeling-related ADAM21 ECM remodeling-related ADAM22 ECM remodeling-related ADAM23 ECM remodeling-related ADAM28 ECM remodeling-related ADAM29 ECM remodeling-related ADAM3 ECM remodeling-related ADAM30 ECM remodeling-related ADAM5 ECM remodeling-related ADAM7 ECM remodeling-related ADAM8 ECM remodeling-related ADAM9 ECM remodeling-related ADAMTS1 ECM remodeling-related ADAMTS10 ECM remodeling-related ADAMTS12 ECM remodeling-related ADAMTS13 ECM remodeling-related ADAMTS14 ECM remodeling-related ADAMTS15 ECM remodeling-related ADAMTS16 ECM remodeling-related ADAMTS17 ECM remodeling-related ADAMTS18 ECM remodeling-related ADAMTS19 ECM remodeling-related ADAMTS2 ECM remodeling-related ADAMTS20 ECM remodeling-related ADAMTS3 ECM remodeling-related ADAMTS4 ECM remodeling-related ADAMTS5 ECM remodeling-related ADAMTS6 ECM remodeling-related ADAMTS7 ECM remodeling-related ADAMTS8 ECM remodeling-related ADAMTS9 ECM remodeling-related ADAMTSL1 ECM remodeling-related ADAMTSL2 ECM remodeling-related ADAMTSL3 ECM remodeling-related ADAMTSL4 ECM remodeling-related ADAMTSL5 ECM remodeling-related AGRIN ECM ALCAM Cell-cell adhesion ANGPT1 Soluble factors and receptors
    [Show full text]
  • Belongs to the TNF Family a New Class of Reverse Signaling
    A New Class of Reverse Signaling Costimulators Belongs to the TNF Family Mingyi Sun and Pamela J. Fink This information is current as J Immunol 2007; 179:4307-4312; ; of September 27, 2021. doi: 10.4049/jimmunol.179.7.4307 http://www.jimmunol.org/content/179/7/4307 References This article cites 85 articles, 38 of which you can access for free at: Downloaded from http://www.jimmunol.org/content/179/7/4307.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision http://www.jimmunol.org/ • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: by guest on September 27, 2021 http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. THE JOURNAL OF IMMUNOLOGY BRIEF REVIEWS A New Class of Reverse Signaling Costimulators Belongs to the TNF Family Mingyi Sun and Pamela J. Fink1 Recent evidence shows that many molecules of the TNF still remains unclear (7). The N-terminal cytoplasmic domains family serve as counter-receptors, inducing costimulation of most TNF family members are conserved across species but through reverse signals in addition to delivering signals not between family members, suggesting that the intracellular through their respective TNF receptors.
    [Show full text]
  • CD95 Ligand - Death Factor and Costimulatory Molecule?
    Cell Death and Differentiation (2003) 10, 1215–1225 & 2003 Nature Publishing Group All rights reserved 1350-9047/03 $25.00 www.nature.com/cdd Review CD95 ligand - death factor and costimulatory molecule? O Janssen*,1, J Qian1, A Linkermann1 and D Kabelitz1 Tissue and Cellular Expression of CD95L 1 Institute for Immunology, Medical Center Schleswig-Holstein, Campus Kiel, Michaelisstrasse 5, D-24105 Kiel, Germany The CD95 ligand (CD95L, Apo-1L, FasL, CD178) is a 281- * Corresponding author: O Janssen. Tel: þ 49-431-5973377; Fax: þ 49-431- amino-acid-containing type II transmembrane protein of the 5973335; E-mail: [email protected] TNF family of death factors (Figure 1).1 Its death-inducing function is best documented in the context of activation- Received 24.4.03; revised 12.6.03; accepted 20.6.03; published online 1 August 2003 induced cell death (AICD) in T cells.2 CD95L is expressed as a Edited by T Ferguson death factor in cytotoxic T lymphocytes (CTL) to kill virally infected or transformed target cells and in natural killer (NK) cells, where it is upregulated by CD16 engagement and 3 Abstract cytokines including IL-2 and IL-12. Similarly, high levels of intracellular CD95L have been detected in monocytic cells The CD95 ligand is involved as a death factor in the with an inducible release upon activation.4 Under physiologi- regulation of activation-induced cell death, establishment cal conditions, CD95L is implicated in the control of erythroid of immune privilege and tumor cell survival. In addition, differentiation,5 angiogenesis in the eye6 and skin home- 7 CD95L may serve as a costimulatory molecule for T-cell ostasis.
    [Show full text]
  • Immunosenescence: a Key Player in Cancer Development Jingyao Lian1,2†, Ying Yue1,2,3†, Weina Yu1,2† and Yi Zhang1,2*
    Lian et al. J Hematol Oncol (2020) 13:151 https://doi.org/10.1186/s13045-020-00986-z REVIEW Open Access Immunosenescence: a key player in cancer development Jingyao Lian1,2†, Ying Yue1,2,3†, Weina Yu1,2† and Yi Zhang1,2* Abstract Immunosenescence is a process of immune dysfunction that occurs with age and includes remodeling of lymphoid organs, leading to changes in the immune function of the elderly, which is closely related to the development of infections, autoimmune diseases, and malignant tumors. T cell–output decline is an important feature of immunose- nescence as well as the production of senescence-associated secretory phenotype, increased glycolysis, and reactive oxygen species. Senescent T cells exhibit abnormal phenotypes, including downregulation of CD27, CD28, and upreg- ulation of CD57, killer cell lectin-like receptor subfamily G, Tim-3, Tight, and cytotoxic T-lymphocyte-associated protein 4, which are tightly related to malignant tumors. The role of immunosenescence in tumors is sophisticated: the many factors involved include cAMP, glucose competition, and oncogenic stress in the tumor microenvironment, which can induce the senescence of T cells, macrophages, natural killer cells, and dendritic cells. Accordingly, these senescent immune cells could also afect tumor progression. In addition, the efect of immunosenescence on the response to immune checkpoint blocking antibody therapy so far is ambiguous due to the low participation of elderly cancer patients in clinical trials. Furthermore, many other senescence-related interventions could be possible with genetic and pharmacological methods, including mTOR inhibition, interleukin-7 recombination, and NAD + activation. Overall, this review aims to highlight the characteristics of immunosenescence and its impact on malignant tumors and immunotherapy, especially the future directions of tumor treatment through senescence-focused strategies.
    [Show full text]
  • Snapshot: Cytokines III Cristina M
    SnapShot: Cytokines III Cristina M. Tato and Daniel J. Cua Schering-Plough Biopharma (Formerly DNAX Research), Palo Alto, CA 94304, USA Cytokine Receptor Source Targets Major Function Disease Association TNFα Murine: Macrophages, Neutrophils, Inflammatory; ↓ = disregulated fever; increased TNFR,p55; TNFR,p75 monocytes, T cells, macrophages, promotes activation susceptibility to bacterial infection; others monocytes, and production of enhanced resistance to LPS-induced septic Human: endothelial cells acute-phase proteins shock TNFR,p60; TNFR,p80 ↑ = exacerbation of arthritis and colitis LTα Murine: T cells, B cells Many cell types Promotes activation ↓ = defective response to bacterial TNFR,p55; TNFR,p75 and cytotoxicity; pathogens; absence of peripheral lymph development of lymph nodes and Peyer’s patches Human: nodes and Peyer’s TNFR,p60; TNFR,p80 patches LTβ LTβR T cells, B cells Myeloid cells, other Peripheral lymph ↓ = increased susceptibility to bacterial cell types node development; infection; absence of lymph nodes and proinflammatory Peyer’s patches ↑ = ectopic lymph node formation LIGHTa LTβR, DcR3, HVEM Activated T cells, B cells, NK cells, Costimulatory; ↓ = defective CD8 T cell costimulation monocytes, DCs DCs, other tissue promotes CTL activity TWEAK Fn14 Monocytes, Tissue progenitors, Proinflammatory; macrophages, epithelial, promotes cell growth endothelial endothelial for tissue repair and remodeling APRIL TACI, BAFF-R, BCMA Macrophages, DCs B cell subsets Promotes T cell- ↓ = impaired class switching to IgA independent
    [Show full text]
  • Molecular Biology of Hodgkin Lymphoma
    Leukemia (2021) 35:968–981 https://doi.org/10.1038/s41375-021-01204-6 REVIEW ARTICLE Lymphoma Molecular biology of Hodgkin lymphoma 1 1 Marc A. Weniger ● Ralf Küppers Received: 17 November 2020 / Revised: 1 February 2021 / Accepted: 18 February 2021 / Published online: 8 March 2021 © The Author(s) 2021. This article is published with open access Abstract Classical Hodgkin lymphoma (cHL) is unique among lymphoid malignancies in several key biological features. (i) The Hodgkin and Reed-Sternberg (HRS) tumor cells are rare among an extensive and complex microenvironment. (ii) They derive from B cells, but have largely lost the B-cell typical gene expression program. (iii) Their specific origin appears to be pre-apoptotic germinal center (GC) B cells. (iv) They consistently develop bi- or multinucleated Reed-Sternberg cells from mononuclear Hodgkin cells. (v) They show constitutive activation of numerous signaling pathways. Recent studies have begun to uncover the basis of these specific features of cHL: HRS cells actively orchestrate their complex microenvironment and attract many distinct subsets of immune cells into the affected tissues, to support their survival and proliferation, and to create an immunosuppressive environment. Reed-Sternberg cells are generated by incomplete cytokinesis and refusion of Hodgkin cells. Epstein-Barr virus (EBV) plays a major role in the rescue of crippled GC B cells 1234567890();,: 1234567890();,: from apoptosis and hence is a main player in early steps of lymphomagenesis of EBV+ cHL cases. The analysis of the landscape of genetic lesions in HRS cells so far did not reveal any highly recurrent HRS cell-specific lesions, but major roles of genetic lesions in members of the NF-κB and JAK/STAT pathways and of factors of immune evasion.
    [Show full text]
  • Identification of Novel CD4+ T Cell Subsets in the Target Tissue Of
    Identification of Novel CD4+ T Cell Subsets in the Target Tissue of Sjögren's Syndrome and Their Differential Regulation by the Lymphotoxin/LIGHT Signaling Axis This information is current as of October 2, 2021. Scott Haskett, Jian Ding, Wei Zhang, Alice Thai, Patrick Cullen, Shanqin Xu, Britta Petersen, Galina Kuznetsov, Luke Jandreski, Stefan Hamann, Taylor L. Reynolds, Norm Allaire, Timothy S. Zheng and Michael Mingueneau J Immunol 2016; 197:3806-3819; Prepublished online 7 Downloaded from October 2016; doi: 10.4049/jimmunol.1600407 http://www.jimmunol.org/content/197/10/3806 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2016/10/06/jimmunol.160040 Material 7.DCSupplemental References This article cites 46 articles, 8 of which you can access for free at: http://www.jimmunol.org/content/197/10/3806.full#ref-list-1 Why The JI? Submit online. by guest on October 2, 2021 • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved.
    [Show full text]
  • Immunity in the Developing Lung Foxa2 Programs Th2 Cell-Mediated
    Foxa2 Programs Th2 Cell-Mediated Innate Immunity in the Developing Lung Gang Chen, Huajing Wan, Fengming Luo, Liqian Zhang, Yan Xu, Ian Lewkowich, Marsha Wills-Karp and Jeffrey A. This information is current as Whitsett of September 27, 2021. J Immunol 2010; 184:6133-6141; Prepublished online 5 May 2010; doi: 10.4049/jimmunol.1000223 http://www.jimmunol.org/content/184/11/6133 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2010/05/05/jimmunol.100022 Material 3.DC1 http://www.jimmunol.org/ References This article cites 59 articles, 17 of which you can access for free at: http://www.jimmunol.org/content/184/11/6133.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 27, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2010 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Foxa2 Programs Th2 Cell-Mediated Innate Immunity in the Developing Lung Gang Chen,* Huajing Wan,† Fengming Luo,‡ Liqian Zhang,* Yan Xu,* Ian Lewkowich,x Marsha Wills-Karp,x and Jeffrey A.
    [Show full text]