Publications
268 results found
Hsieh C-S, Macatonia SE, Tripp CS, et al., 2008, Development of T<sub>H</sub>1 CD4<SUP>+</SUP> T cells through IL-12 produced by <i>Listeria</i>-induced macrophages, JOURNAL OF IMMUNOLOGY, Vol: 181, Pages: 4437-4439, ISSN: 0022-1767
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- Citations: 8
Hsieh C-S, Macatonia SE, Tripp CS, et al., 2008, Pillars article: development of TH1 CD4+ T cells through IL-12 produced by Listeria-induced macrophages. 1993. Science 260(5107): 547-549., J Immunol, Vol: 181, Pages: 4437-4439
O'Garra A, Barrat FJ, Castro AG, et al., 2008, Strategies for use of IL-10 or its antagonists in human disease, IMMUNOLOGICAL REVIEWS, Vol: 223, Pages: 114-131, ISSN: 0105-2896
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- Citations: 325
O'Garra A, Stockinger B, Veldhoen M, 2008, Differentiation of human T<sub>H</sub>-17 cells does require TGF-β!, NATURE IMMUNOLOGY, Vol: 9, Pages: 588-590, ISSN: 1529-2908
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- Citations: 78
Kassiotis G, O'Garra A, 2008, Immunology - Immunity benefits from a little suppression, SCIENCE, Vol: 320, Pages: 1168-1169, ISSN: 0036-8075
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- Citations: 10
Boonstra A A, Trinchieri G G, O'Garra A A, 2008, The Plasticity of Dendritic Cells Populations in Promoting Th-cell Responses, Handbook of Dendritic Cells, Pages: 385-403, ISBN: 9783527311095
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- Citations: 1
Rajsbaum R, Stoye JP, O'Garra A, 2008, Type I interferon-dependent and -independent expression of tripartite motif proteins in immune cells, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 38, Pages: 619-630, ISSN: 0014-2980
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- Citations: 127
Rousseau S, Papoutsopoulou M, Symons A, et al., 2008, TPL2-mediated activation of ERK1 and ERK2 regulates the processing of pre-TNFα in LPS-stimulated macrophages, JOURNAL OF CELL SCIENCE, Vol: 121, Pages: 149-154, ISSN: 0021-9533
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- Citations: 107
Vieira P, O'Garra A, 2007, Regula'ten' the gut., Nat Immunol, Vol: 8, Pages: 905-907, ISSN: 1529-2908
Vieira P, O'Garra A, 2007, Regula'ten' the gut, NATURE IMMUNOLOGY, Vol: 8, Pages: 905-907, ISSN: 1529-2908
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- Citations: 19
O'Garra A, Vieira P, 2007, T<sub>H</sub>1 cells control themselves by producing interleukin-10, NATURE REVIEWS IMMUNOLOGY, Vol: 7, Pages: 425-428, ISSN: 1474-1733
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- Citations: 480
Young D, O'Garra A, 2007, Mycobacterium tuberculosis and its ability to resist immunity, Decoding the Genomic Control of Immune Reactions, Pages: 169-180, ISBN: 9780470027554
Resistance to tuberculosis involves a balance between the immune activation required to restrict the infection and the immune regulation required to prevent collateral damage to surrounding tissues. We explore here the hypothesis that genetic diversity of Mycobacterium tuberculosis provides an opportunity to tilt this balance in favour of the pathogen through variations in innate immune signalling.
Young D, O'Garra A, 2007, Mycobacterium tuberculosis and its ability to resist immunity., Novartis Found Symp, Vol: 281, Pages: 169-177, ISSN: 1528-2511
Resistance to tuberculosis involves a balance between the immune activation required to restrict the infection and the immune regulation required to prevent collateral damage to surrounding tissues. We explore here the hypothesis that genetic diversity of Mycobacterium tuberculosis provides an opportunity to tilt this balance in favour of the pathogen through variations in innate immune signalling.
Boonstra A, Rajsbaum R, Holman M, et al., 2006, Macrophages and myeloid dendritic cells, but not plasmacytoid dendritic cells, produce IL-10 in response to MyD88- and TRIF-dependent TLR signals, and TLR-independent signals, JOURNAL OF IMMUNOLOGY, Vol: 177, Pages: 7551-7558, ISSN: 0022-1767
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- Citations: 231
Rowland CA, Lertmemongkolchai G, Bancroft A, et al., 2006, Critical role of type 1 cytokines in controlling initial infection with <i>Burkholderia mallei</i>, INFECTION AND IMMUNITY, Vol: 74, Pages: 5333-5340, ISSN: 0019-9567
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- Citations: 30
Neighbors M, Hartley SB, Xu X, et al., 2006, Breakpoints in immunoregulation required for Th1 cells to induce diabetes, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 36, Pages: 2315-2323, ISSN: 0014-2980
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- Citations: 16
Sponaas A-M, Cadman ET, Voisine C, et al., 2006, Malaria infection changes the ability of splenic dendritic cell populations to stimulate antigen-specific T cells, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 203, Pages: 1427-1433, ISSN: 0022-1007
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- Citations: 126
Papoutsopoulou S, Symons A, Tharmalingham T, et al., 2006, ABIN-2 is required for optimal activation of Erk MAP kinase in innate immune responses, NATURE IMMUNOLOGY, Vol: 7, Pages: 606-615, ISSN: 1529-2908
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- Citations: 71
Shoemaker J, Saraiva M, O'Garra A, 2006, GATA-3 directly remodels the <i>IL-10</i> locus independently of IL-4 in CD4<SUP>+</SUP> T cells, JOURNAL OF IMMUNOLOGY, Vol: 176, Pages: 3470-3479, ISSN: 0022-1767
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- Citations: 126
Haque A, Easton A, Smith D, et al., 2006, Role of T cells in innate and adaptive immunity against murine <i>Burkholderia pseudomallei</i> infection, JOURNAL OF INFECTIOUS DISEASES, Vol: 193, Pages: 370-379, ISSN: 0022-1899
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- Citations: 94
Xystrakis E, Kusumaker S, Boswell S, et al., 2006, Reversing the defective induction of IL-10-secreting regulatory T cells in glucocorticoid-resistant asthma patients, J Clin Invest, Vol: 116, Pages: 146-155
O'Garra A, 2005, Development and function of IL-10-secreting regulatory T cells: Comparison with naturally occurring CD4<sup>+</sup>CD25<sup>+</sup> regulatory T cells, International Congress Series, Vol: 1285, Pages: 160-168, ISSN: 0531-5131
Regulatory T cells (TReg) control immune responses to self and nonself Ags. The relationship between Ag-driven IL-10-secreting TReg (IL-10-TReg) and naturally occurring CD4 CD25 TReg is as yet unclear. We show that mouse IL-10-TReg obtained using either in vitro or in vivo regimens of antigenic stimulation did not express the CD4 CD25 TReg-associated transcription factor Foxp3. However, despite the absence of Foxp3 expression, homogeneous populations of IL-10-TReg inhibited the in vitro proliferation of CD4 CD25 T cells with a similar efficiency to that of CD4 CD25 TReg. This inhibition of T cell proliferation by IL-10-TReg was achieved through an IL-10-independent mechanism as seen for CD4 CD25 TReg and was overcome by exogenous IL-2. Both IL-10-TReg and CD4 CD25 TReg were similar in that they produced little to no IL-2. These data show that Foxp3 expression is not a prerequisite for IL-10-TReg activity in vitro or in vivo and suggest that IL-10-TReg and naturally occurring CD4 CD25 TReg may have distinct origins. Thus, these different regulatory populations may have different roles at different stages of the immune response. © 2005.
Saraiva M, Christensen JR, Tsytsykova AV, et al., 2005, Identification of a macrophage-specific chromatin signature in the IL-10 locus, JOURNAL OF IMMUNOLOGY, Vol: 175, Pages: 1041-1046, ISSN: 0022-1767
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- Citations: 105
Okada T, Miller MJ, Parker I, et al., 2005, Antigen-engaged B cells undergo chemotaxis toward the T zone and form motile conjugates with helper T cells, PLOS BIOLOGY, Vol: 3, Pages: 1047-1061, ISSN: 1545-7885
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- Citations: 430
Asselin-Paturel C, Brizard G, Chemin K, et al., 2005, Type I interferon dependence of plasmacytoid dendritic cell activation and migration., J Exp Med, Vol: 201, Pages: 1157-1167, ISSN: 0022-1007
Differential expression of Toll-like receptor (TLR) by conventional dendritic cells (cDCs) and plasmacytoid DC (pDCs) has been suggested to influence the type of immune response induced by microbial pathogens. In this study we show that, in vivo, cDCs and pDCs are equally activated by TLR4, -7, and -9 ligands. Type I interferon (IFN) was important for pDC activation in vivo in response to all three TLR ligands, whereas cDCs required type I IFN signaling only for TLR9- and partially for TLR7-mediated activation. Although TLR ligands induced in situ migration of spleen cDC into the T cell area, spleen pDCs formed clusters in the marginal zone and in the outer T cell area 6 h after injection of TLR9 and TLR7 ligands, respectively. In vivo treatment with TLR9 ligands decreased pDC ability to migrate ex vivo in response to IFN-induced CXCR3 ligands and increased their response to CCR7 ligands. Unlike cDCs, the migration pattern of pDCs required type I IFN for induction of CXCR3 ligands and responsiveness to CCR7 ligands. These data demonstrate that mouse pDCs differ from cDCs in the in vivo response to TLR ligands, in terms of pattern and type I IFN requirement for activation and migration.
Asselin-Paturel C, Brizard G, Chemin K, et al., 2005, Type I interferon dependence of plasmacytoid dendritic cell activation and migration, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 201, Pages: 1157-1167, ISSN: 0022-1007
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- Citations: 270
Hawrylowicz CM, O'Garra A, 2005, Potential role of interleukin-10-secreting regulatory T cells in allergy and asthma, NATURE REVIEWS IMMUNOLOGY, Vol: 5, Pages: 271-283, ISSN: 1474-1733
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- Citations: 514
Barthlott T, Moncrieffe H, Veldhoen M, et al., 2005, CD25<SUP>+</SUP>CD4<SUP>+</SUP> T cells compete with naive CD4<SUP>+</SUP> T cells for IL-2 and exploit it for the induction of IL-10 production, INTERNATIONAL IMMUNOLOGY, Vol: 17, Pages: 279-288, ISSN: 0953-8178
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- Citations: 150
O'Garra A, Trinchieri G, 2004, Are dendritic cells afraid of commitment?, NATURE IMMUNOLOGY, Vol: 5, Pages: 1206-1208, ISSN: 1529-2908
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- Citations: 19
O'Garra A, Vieira PL, Vieira P, et al., 2004, IL-10-producing and naturally occurring CD4+ Tregs: limiting collateral damage., J Clin Invest, Vol: 114, Pages: 1372-1378, ISSN: 0021-9738
Effective immune responses against pathogens are sometimes accompanied by strong inflammatory reactions. To minimize damage to self, the activation of the immune system also triggers anti-inflammatory circuits. Both inflammatory and anti-inflammatory reactions are normal components of the same immune response, which coordinately fight infections while preventing immune pathology. IL-10 is an important suppressive cytokine, produced by a large number of immune cells in addition to the antigen-driven IL-10-producing regulatory and the naturally occurring suppressor CD4+ T cells, which is a key player in anti-inflammatory immune responses. However, additional mechanisms have evolved to ensure that pathogen eradication is achieved with minimum damage to the host. Here we discuss those mechanisms that operate to regulate effector immune responses.
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