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Dive into the research topics where Jordi Ochando is active.

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Featured researches published by Jordi Ochando.


Nature Immunology | 2006

Alloantigen-presenting plasmacytoid dendritic cells mediate tolerance to vascularized grafts.

Jordi Ochando; Chiho Homma; Yu Yang; Andrés Hidalgo; Alexandre Garin; Frank Tacke; Veronique Angeli; Yansui Li; Peter Boros; Yaozhong Ding; Rolf Jessberger; Giorgio Trinchieri; Sergio A. Lira; Gwendalyn J. Randolph; Jonathan S. Bromberg

The induction of alloantigen-specific unresponsiveness remains an elusive goal in organ transplantation. Here we identify plasmacytoid dendritic cells (pDCs) as phagocytic antigen-presenting cells essential for tolerance to vascularized cardiac allografts. Tolerizing pDCs acquired alloantigen in the allograft and then moved through the blood to home to peripheral lymph nodes. In the lymph node, alloantigen-presenting pDCs induced the generation of CCR4+CD4+CD25+Foxp3+ regulatory T cells (Treg cells). Depletion of pDCs or prevention of pDC lymph node homing inhibited peripheral Treg cell development and tolerance induction, whereas adoptive transfer of tolerized pDCs induced Treg cell development and prolonged graft survival. Thus, alloantigen-presenting pDCs home to the lymph nodes in tolerogenic conditions, where they mediate alloantigen-specific Treg cell development and allograft tolerance.


Journal of Experimental Medicine | 2007

Blood-derived dermal langerin+ dendritic cells survey the skin in the steady state

Florent Ginhoux; Matthew Collin; Milena Bogunovic; Michal Abel; Marylene Leboeuf; Julie Helft; Jordi Ochando; Adrien Kissenpfennig; Bernard Malissen; Marcos Grisotto; Hans Snoeck; Gwendalyn J. Randolph; Miriam Merad

Langerin is a C-type lectin receptor that recognizes glycosylated patterns on pathogens. Langerin is used to identify human and mouse epidermal Langerhans cells (LCs), as well as migratory LCs in the dermis and the skin draining lymph nodes (DLNs). Using a mouse model that allows conditional ablation of langerin+ cells in vivo, together with congenic bone marrow chimeras and parabiotic mice as tools to differentiate LC- and blood-derived dendritic cells (DCs), we have revisited the origin of langerin+ DCs in the skin DLNs. Our results show that in contrast to the current view, langerin+CD8− DCs in the skin DLNs do not derive exclusively from migratory LCs, but also include blood-borne langerin+ DCs that transit through the dermis before reaching the DLN. The recruitment of circulating langerin+ DCs to the skin is dependent on endothelial selectins and CCR2, whereas their recruitment to the skin DLNs requires CCR7 and is independent of CD62L. We also show that circulating langerin+ DCs patrol the dermis in the steady state and migrate to the skin DLNs charged with skin antigens. We propose that this is an important and previously unappreciated element of immunosurveillance that needs to be taken into account in the design of novel vaccine strategies.


Immunity | 2009

Regulatory T cells sequentially migrate from inflamed tissues to draining lymph nodes to suppress the alloimmune response.

Nan Zhang; Bernd Schröppel; Girdhari Lal; Claudia Jakubzick; Xia Mao; Dan Chen; Na Yin; Rolf Jessberger; Jordi Ochando; Yaozhong Ding; Jonathan S. Bromberg

To determine the site and mechanism of suppression by regulatory T (Treg) cells, we investigated their migration and function in an islet allograft model. Treg cells first migrated from blood to the inflamed allograft where they were essential for the suppression of alloimmunity. This process was dependent on the chemokine receptors CCR2, CCR4, and CCR5 and P- and E-selectin ligands. In the allograft, Treg cells were activated and subsequently migrated to the draining lymph nodes (dLNs) in a CCR2, CCR5, and CCR7 fashion; this movement was essential for optimal suppression. Treg cells inhibited dendritic cell migration in a TGF-beta and IL-10 dependent fashion and suppressed antigen-specific T effector cell migration, accumulation, and proliferation in dLNs and allografts. These results showed that sequential migration from blood to the target tissue and to dLNs is required for Treg cells to differentiate and execute fully their suppressive function.


Nature Immunology | 2008

The sphingosine 1-phosphate receptor 1 causes tissue retention by inhibiting the entry of peripheral tissue T lymphocytes into afferent lymphatics

Levi Ledgerwood; Girdhari Lal; Nan Zhang; Alexandre Garin; Steven J. Esses; Florent Ginhoux; Miriam Merad; Helene Peche; Sergio A. Lira; Yaozhong Ding; Yu Yang; Xingxuan He; Edward H. Schuchman; Maria L. Allende; Jordi Ochando; Jonathan S. Bromberg

Although much is known about the migration of T cells from blood to lymph nodes, less is known about the mechanisms regulating the migration of T cells from tissues into lymph nodes through afferent lymphatics. Here we investigated T cell egress from nonlymphoid tissues into afferent lymph in vivo and developed an experimental model to recapitulate this process in vitro. Agonism of sphingosine 1-phosphate receptor 1 inhibited the entry of tissue T cells into afferent lymphatics in homeostatic and inflammatory conditions and caused the arrest, mediated at least partially by interactions of the integrin LFA-1 with its ligand ICAM-1 and of the integrin VLA-4 with its ligand VCAM-1, of polarized T cells at the basal surface of lymphatic but not blood vessel endothelium. Thus, the increased sphingosine 1-phosphate present in inflamed peripheral tissues may induce T cell retention and suppress T cell egress.


Journal of Immunology | 2005

Lymph Node Occupancy Is Required for the Peripheral Development of Alloantigen-Specific Foxp3+ Regulatory T Cells

Jordi Ochando; Adam C. Yopp; Yu Yang; Alexandre Garin; Yansui Li; Peter Boros; Jaime Llodra; Yaozhong Ding; Sergio A. Lira; Nancy Krieger; Jonathan S. Bromberg

We previously demonstrated that L-selectin (CD62L)-dependent T cell homing to lymph nodes (LN) is required for tolerance induction to alloantigen. To explore the mechanisms of this observation, we analyzed the development and distribution of regulatory T cells (Treg), which play an important protective role against allograft rejection in transplantation tolerance. Alloantigen-specific tolerance was induced using either anti-CD2 plus anti-CD3 mAbs, or anti-CD40L mAbs plus donor-specific transfusion, in fully mismatched (BALB/c donor, C57BL/6 recipient) vascularized cardiac allografts. An expansion of CD4+CD25+CD62Lhigh T cells was observed specifically within the LN of tolerant animals, but not in other anatomic sites or under nontolerizing conditions. These cells exhibited a substantial up-regulation of Foxp3 expression as measured by real-time PCR and by fluorescent immunohistochemistry, and possessed alloantigen-specific suppressor activity. Neither LN nor other lymphoid cells expressed the regulatory phenotype if recipients were treated with anti-CD62L mAbs, which both prevented LN homing and caused early allograft rejection. However, administration of FTY720, a sphingosine 1-phosphate receptor modulator that induces CD62L-independent T cell accumulation in the LNs, restored CD4+CD25+ Treg in the LNs along with graft survival. These data suggest that alloantigen-specific Foxp3+CD4+CD25+ Treg develop and are required within the LNs during tolerization, and provide compelling evidence that distinct lymphoid compartments play critical roles in transplantation tolerance.


Nature Immunology | 2016

New insights into the multidimensional concept of macrophage ontogeny, activation and function

Florent Ginhoux; Joachim L. Schultze; Peter J. Murray; Jordi Ochando; Subhra K. Biswas

Macrophages have protective roles in immunity to pathogens, tissue development, homeostasis and repair following damage. Maladaptive immunity and inflammation provoke changes in macrophage function that are causative of disease. Despite a historical wealth of knowledge about macrophages, recent advances have revealed unknown aspects of their development and function. Following development, macrophages are activated by diverse signals. Such tissue microenvironmental signals together with epigenetic changes influence macrophage development, activation and functional diversity, with consequences in disease and homeostasis. We discuss here how recent discoveries in these areas have led to a multidimensional concept of macrophage ontogeny, activation and function. In connection with this, we also discuss how technical advances facilitate a new roadmap for the isolation and analysis of macrophages at high resolution.


Journal of Immunology | 2009

c-Maf Regulates IL-10 Expression during Th17 Polarization

Jiangnan Xu; Yu Yang; Guixing Qiu; Girdhari Lal; Zhihong Wu; David E. Levy; Jordi Ochando; Jonathan S. Bromberg; Yaozhong Ding

IL-10 production by Th17 cells is critical for limiting autoimmunity and inflammatory responses. Gene array analysis on Stat6 and T-bet double-deficient Th17 cells identified the Th2 transcription factor c-Maf to be synergistically up-regulated by IL-6 plus TGFβ and associated with Th17 IL-10 production. Both c-Maf and IL-10 induction during Th17 polarization depended on Stat3, but not Stat6 or Stat1, and mechanistically differed from IL-10 regulation by Th2 or IL-27 signals. TGFβ was also synergistic with IL-27 to induce c-Maf, and it induced Stat1-independent IL-10 expression in contrast to IL-27 alone. Retroviral transduction of c-Maf was able to induce IL-10 expression in Stat6-deficient CD4 and CD8 T cells, and c-Maf directly transactivated IL-10 gene expression through binding to a MARE (Maf recognition element) motif in the IL-10 promoter. Taken together, these data reveal a novel role for c-Maf in regulating T effector development, and they suggest that TGFβ may antagonize Th17 immunity by IL-10 production through c-Maf induction.


Journal of Clinical Investigation | 2010

Monocytic suppressive cells mediate cardiovascular transplantation tolerance in mice

Mercedes Rodriguez Garcia; Levi G. Ledgerwood; Yu Yang; Jiangnan Xu; Girdhari Lal; Bryna E. Burrell; Ge Ma; Daigo Hashimoto; Yansui Li; Peter Boros; Marcos G. Grisotto; Nico van Rooijen; Rafael Matesanz; Frank Tacke; Florent Ginhoux; Yaozhong Ding; Shu-Hsia Chen; Gwendalyn J. Randolph; Miriam Merad; Jonathan S. Bromberg; Jordi Ochando

One of the main unresolved questions in solid organ transplantation is how to establish indefinite graft survival that is free from long-term treatment with immunosuppressive drugs and chronic rejection (i.e., the establishment of tolerance). The failure to achieve this goal may be related to the difficulty in identifying the phenotype and function of the cell subsets that participate in the induction of tolerance. To address this issue, we investigated the suppressive roles of recipient myeloid cells that may be manipulated to induce tolerance to transplanted hearts in mice. Using depleting mAbs, clodronate-loaded liposomes, and transgenic mice specific for depletion of CD11c+, CD11b+, or CD115+ cells, we identified a tolerogenic role for CD11b+CD115+Gr1+ monocytes during the induction of tolerance by costimulatory blockade with CD40L-specific mAb. Early after transplantation, Gr1+ monocytes migrated from the bone marrow into the transplanted organ, where they prevented the initiation of adaptive immune responses that lead to allograft rejection and participated in the development of Tregs. Our results suggest that mobilization of bone marrow CD11b+CD115+Gr1+ monocytes under sterile inflammatory conditions mediates the induction of indefinite allograft survival. We propose that manipulating the common bone marrow monocyte progenitor could be a useful clinical therapeutic approach for inducing transplantation tolerance.


Cell Reports | 2012

Immune Tolerance to Tumor Antigens Occurs in a Specialized Environment of the Spleen

Stefano Ugel; Elisa Peranzoni; Giacomo Desantis; Mariacristina Chioda; Steffen Walter; Toni Weinschenk; Jordi Ochando; Anna Cabrelle; Susanna Mandruzzato; Vincenzo Bronte

Peripheral tolerance to tumor antigens (Ags) is a major hurdle for antitumor immunity. Draining lymph nodes are considered the privileged sites for Ag presentation to T cells and for the onset of peripheral tolerance. Here, we show that the spleen is fundamentally important for tumor-induced tolerance. Splenectomy restores lymphocyte function and induces tumor regression when coupled with immunotherapy. Splenic CD11b(+)Gr-1(int)Ly6C(hi) cells, mostly comprising proliferating CCR2(+)-inflammatory monocytes with features of myeloid progenitors, expand in the marginal zone of the spleen. Here, they alter the normal tissue cytoarchitecture and closely associate with memory CD8(+) T cells, cross-presenting tumor Ags and causing their tolerization. Because of its high proliferative potential, this myeloid cell subset is also susceptible to low-dose chemotherapy, which can be exploited as an adjuvant to passive immunotherapy. CCL2 serum levels in cancer patients are directly related to the accumulation of immature myeloid cells and are predictive for overall survival in patients who develop a multipeptide response to cancer vaccines.


Journal of Experimental Medicine | 2011

Pretransplant CSF-1 therapy expands recipient macrophages and ameliorates GVHD after allogeneic hematopoietic cell transplantation

Daigo Hashimoto; Andrew Chow; Melanie Greter; Yvonne Saenger; Wing Hong Kwan; Marylene Leboeuf; Florent Ginhoux; Jordi Ochando; Yuya Kunisaki; Nico van Rooijen; Chen Liu; Takanori Teshima; Peter S. Heeger; E. Richard Stanley; Paul S. Frenette; Miriam Merad

Host macrophages protect against graft-versus-host disease in part by engulfing donor T cells and inhibiting their proliferation.

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Yu Yang

Icahn School of Medicine at Mount Sinai

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Adam C. Yopp

Icahn School of Medicine at Mount Sinai

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Peter Boros

Icahn School of Medicine at Mount Sinai

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Sergio A. Lira

Icahn School of Medicine at Mount Sinai

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Florent Ginhoux

Icahn School of Medicine at Mount Sinai

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Levi Ledgerwood

Icahn School of Medicine at Mount Sinai

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Miriam Merad

Icahn School of Medicine at Mount Sinai

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Patricia Conde

Icahn School of Medicine at Mount Sinai

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