IL-4 Production from Basophils IL-3-Induced M 2 Macrophages by Inhibiting SHIP Represses the Generation of Antov

[1]  H. Karasuyama,et al.  Fc receptor γ-chain, a constitutive component of the IL-3 receptor, is required for IL-3-induced IL-4 production in basophils , 2009, Nature Immunology.

[2]  H. Langen,et al.  Human basophils activated by mast cell-derived IL-3 express retinaldehyde dehydrogenase-II and produce the immunoregulatory mediator retinoic acid. , 2008, Blood.

[3]  D. MacGlashan Granulocytes: New roles for basophils , 2008, Immunology and cell biology.

[4]  G. Dranoff,et al.  IL-3 is required for increases in blood basophils in nematode infection in mice and can enhance IgE-dependent IL-4 production by basophils in vitro , 2008, Laboratory Investigation.

[5]  P. Allavena,et al.  Macrophage polarization in tumour progression. , 2008, Seminars in cancer biology.

[6]  J. Urban,et al.  T cell-derived IL-3 plays key role in parasite infection-induced basophil production but is dispensable for in vivo basophil survival. , 2008, International immunology.

[7]  J. Hamilton Colony-stimulating factors in inflammation and autoimmunity , 2008, Nature Reviews Immunology.

[8]  Takao Shimizu,et al.  Basophils play a pivotal role in immunoglobulin-G-mediated but not immunoglobulin-E-mediated systemic anaphylaxis. , 2008, Immunity.

[9]  P. Allavena,et al.  The Yin‐Yang of tumor‐associated macrophages in neoplastic progression and immune surveillance , 2008, Immunological reviews.

[10]  T. Kawakami,et al.  Regulation of myeloproliferation and M2 macrophage programming in mice by Lyn/Hck, SHIP, and Stat5. , 2008, The Journal of clinical investigation.

[11]  Ruslan Medzhitov,et al.  A mechanism for the initiation of allergen-induced T helper type 2 responses , 2008, Nature Immunology.

[12]  W. Paul,et al.  Basophils and type 2 immunity , 2008, Current opinion in hematology.

[13]  Alberto Mantovani,et al.  Macrophage activation and polarization. , 2008, Frontiers in bioscience : a journal and virtual library.

[14]  S. Uematsu,et al.  IL‐3 is an important differentiation factor for the development of prostaglandin E2‐producing macrophages between C57BL/6 and BALB/c mice , 2007, European journal of immunology.

[15]  S. Albelda,et al.  Cross-Talk between Myeloid-Derived Suppressor Cells and Macrophages Subverts Tumor Immunity toward a Type 2 Response1 , 2007, The Journal of Immunology.

[16]  H. Katz,et al.  Inhibition of pathologic inflammation by leukocyte Ig‐like receptor B4 and related inhibitory receptors , 2007, Immunological reviews.

[17]  A. Burgess,et al.  Mice Lacking Three Myeloid Colony-Stimulating Factors (G-CSF, GM-CSF, and M-CSF) Still Produce Macrophages and Granulocytes and Mount an Inflammatory Response in a Sterile Model of Peritonitis1 , 2007, The Journal of Immunology.

[18]  T. Lawrence,et al.  Granulocyte-Macrophage Colony-Stimulating Factor (CSF) and Macrophage CSF-Dependent Macrophage Phenotypes Display Differences in Cytokine Profiles and Transcription Factor Activities: Implications for CSF Blockade in Inflammation1 , 2007, The Journal of Immunology.

[19]  M. Olszewski,et al.  Role of granulocyte macrophage colony-stimulating factor in host defense against pulmonary Cryptococcus neoformans infection during murine allergic bronchopulmonary mycosis. , 2007, The American journal of pathology.

[20]  James J. Lee,et al.  When is a mouse basophil not a basophil? , 2007, Blood.

[21]  A. Sica,et al.  p50 nuclear factor-kappaB overexpression in tumor-associated macrophages inhibits M1 inflammatory responses and antitumor resistance. , 2006, Cancer research.

[22]  R. Schwendener,et al.  Clodronate-liposome-mediated depletion of tumour-associated macrophages: a new and highly effective antiangiogenic therapy approach , 2006, British Journal of Cancer.

[23]  D. Hebenstreit,et al.  Signaling mechanisms, interaction partners, and target genes of STAT6. , 2006, Cytokine & growth factor reviews.

[24]  C. Liu,et al.  Targeting tumor-associated macrophages as a novel strategy against breast cancer. , 2006, The Journal of clinical investigation.

[25]  Hua Yu,et al.  Inhibiting Stat3 signaling in the hematopoietic system elicits multicomponent antitumor immunity , 2005, Nature Medicine.

[26]  T. Hibi,et al.  Abnormally Differentiated Subsets of Intestinal Macrophage Play a Key Role in Th1-Dominant Chronic Colitis through Excess Production of IL-12 and IL-23 in Response to Bacteria1 , 2005, The Journal of Immunology.

[27]  A. Mantovani,et al.  Targeting myelomonocytic cells to revert inflammation-dependent cancer promotion. , 2005, Cancer research.

[28]  A. Mui,et al.  SHIP represses the generation of alternatively activated macrophages. , 2005, Immunity.

[29]  Takashi Saito,et al.  Negative control of basophil expansion by IRF-2 critical for the regulation of Th1/Th2 balance. , 2005, Blood.

[30]  R. Thurmond,et al.  Organic cation transporter 3 modulates murine basophil functions by controlling intracellular histamine levels , 2005, The Journal of experimental medicine.

[31]  G. Trinchieri,et al.  Redirecting in vivo elicited tumor infiltrating macrophages and dendritic cells towards tumor rejection. , 2005, Cancer research.

[32]  P. Sinha,et al.  Reduction of Myeloid-Derived Suppressor Cells and Induction of M1 Macrophages Facilitate the Rejection of Established Metastatic Disease1 , 2005, The Journal of Immunology.

[33]  Silvano Sozzani,et al.  The chemokine system in diverse forms of macrophage activation and polarization. , 2004, Trends in immunology.

[34]  G. Krystal,et al.  SHIP, SHIP2, and PTEN activities are regulated in vivo by modulation of their protein levels: SHIP is up-regulated in macrophages and mast cells by lipopolysaccharide. , 2003, Experimental hematology.

[35]  Margarita Martinez-Moczygemba,et al.  Biology of common β receptor–signaling cytokines: IL-3, IL-5, and GM-CSF , 2003 .

[36]  M. Huber,et al.  The role of SHIP in cytokine-induced signaling. , 2003, Reviews of physiology, biochemistry and pharmacology.

[37]  J. Schroeder,et al.  Basophils in airway disease , 2002, Current allergy and asthma reports.

[38]  S. Akira,et al.  STAT5 Induces Macrophage Differentiation of M1 Leukemia Cells Through Activation of IL-6 Production Mediated by NF-κB p651 , 2001, The Journal of Immunology.

[39]  J. Whitsett,et al.  GM-CSF regulates alveolar macrophage differentiation and innate immunity in the lung through PU.1. , 2001, Immunity.

[40]  C. Tadokoro,et al.  Bone marrow-derived macrophages grown in GM-CSF or M-CSF differ in their ability to produce IL-12 and to induce IFN-gamma production after stimulation with Trypanosoma cruzi antigens. , 2001, Immunology letters.

[41]  Andrew V. Nguyen,et al.  Colony-Stimulating Factor 1 Promotes Progression of Mammary Tumors to Malignancy , 2001, The Journal of experimental medicine.

[42]  M. Grusby,et al.  Cutting Edge: STAT6-Deficient Mice Have Enhanced Tumor Immunity to Primary and Metastatic Mammary Carcinoma1 , 2000, The Journal of Immunology.

[43]  C. Schindler,et al.  Myeloid differentiation of FdCP1 cells is dependent on Stat5 processing. , 2000, Blood.

[44]  D. Harlan,et al.  Susceptibility or resistance to Leishmania infection is dictated by the macrophages evolved under the influence of IL‐3 or GM‐CSF , 1999, European journal of immunology.

[45]  F. Lemoine,et al.  IL-3-induced coexpression of histidine decarboxylase, IL-4 and IL-6 mRNA by murine basophil precursors. , 1999, Experimental hematology.

[46]  A. Dunn,et al.  Granulocyte/macrophage colony-stimulating factor-deficient mice show no major perturbation of hematopoiesis but develop a characteristic pulmonary pathology. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[47]  R. Coffman,et al.  Leishmania antigens presented by GM-CSF-derived macrophages protect susceptible mice against challenge with Leishmania major. , 1993, Journal of immunology.

[48]  J. Ihle,et al.  Interleukin-3 and hematopoiesis. , 1992, Chemical immunology.