Luis Roberto Benghi Soares

Pós-doutorado

Idiomas

Áreas de atuação

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Produções bibliográficas

• SOARES, Luis ; Weffort-Santos, Almeriane M ; FATHMAN, Cg ; Soares, Luis RB . Dengue-2 Structural Proteins Associate with Human Proteins to Produce a Coagulation and Innate Immune Response Biased Interactome. BMC Infectious Diseases (Online) , v. 11, p. 34, 2011.

• LINEBERRY, Neil ; Su L ; SOARES, Luis ; FATHMAN, Cg . The single subunit transmembrane E3 ligase gene related to anergy in lymphocytes (GRAIL) captures and then ubiquitinates transmembrane proteins across the cell membrane. Journal of Biological Chemistry (Online) , v. 283, p. 28497-28505, 2008.

• Keiichi Kodama ; Atul J Butte ; Remi J Creusot ; Su L ; Deqiao Sheng ; SOARES, Luis ; FATHMAN, Cg . Tissue- and age-specific changes in gene expression during disease induction and progression in NOD mice.. Clinical Immunology (Orlando) , v. 129, p. 179-191, 2008.

• Su L ; LINEBERRY, Neil ; SOARES, Luis ; FATHMAN, Cg . A novel E3 ubiquitin ligase substrate screen identifies Rho guanine dissociation inhibitor as a substrate of gene related to anergy in lymphocytes.. Journal of Immunology (Baltimore) , v. 177, p. 7559-7566, 2006.

• FATHMAN, Cg ; SOARES, Luis ; Chan SM ; Utz PJ . An array of possibilities for the study of autoimmunity.. Nature (London) , v. 435, p. 605-611, 2005.

• Mobin Karimi ; SOARES, Luis ; Robert Negrin . Silencing human NKG2D, DAP10, and DAP12 reduces cytotoxicity of activated CD8+ T cells and NK cells. Journal of Immunology (Baltimore) , v. 175, p. 7819-7828, 2005.

• ENGLEMAN, Edgar ; BRODY, Joshua ; SOARES, Luis . Using signaling pathways to overcome immune tolerance to tumors.. Science , USA, v. 241, p. pe28-30, 2004.

• SOARES, Luis ; K, Furumoto ; E,, Engleman ; M, Merad . Induction of potent antitumor immunity by in situ targeting of intratumoral DCs.. Journal of Clinical Investigation , USA, v. 113, n.5, p. 774-783, 2004.

• SOARES, Luis ; FATHMAN, Cg . Two isoforms of otubain 1 regulate T cell anergy via GRAIL.. Nature Immunology , USA, v. 5, n.1, p. 45-54, 2004.

• SEROOGY, Christine ; SOARES, Luis ; FATHMAN, Cg . The gene related to anergy in lymphocytes, an E3 ubiquitin ligase, is necessary for. Journal of Immunology (Baltimore) , USA, v. 173, n.1, p. 79-85, 2004.

• N, Anandasabapathy ; FATHMAN, Cg ; SOARES, Luis . GR AIL: A novel E3 ubiquitin ligase that inhibits cytokine gene transcription is expressed in anergic CD4+ T cells.. Immunity (Cambridge) , USA, v. April, n.18, p. 535-547, 2003.

• SOARES, Luis ; ENGLEMAN, Edgar . V7 (CD101) ligation inhibits TCR/CD3-induced IL-2 production by blocking Ca2+ flux and nuclear factor of activated T cell nuclear translocation.. Journal of Immunology (Baltimore) , USA, v. 161, n.1, p. 209-217, 1998.

• SOARES, Luis ; BENICHOU, Gilles . Differential activation of T cells by natural antigen peptide analogues: influence on autoimmune and alloimmune in vivo T cell responses. . Journal of Immunology (Baltimore) , USA, v. 160, n.10, p. 4768-4775, 1998.

• SOARES, Luis ; ENGLEMAN, Edgar . Ligation of the V7 molecule on T cells blocks anergy induction through a CD28-independent mechanism. Journal of Investigational Allergology & Clinical Immunology , USA, v. 159, n.3, p. 1115-1124, 1997.

• SOARES, Luis ; ENGLEMAN, Edgar . Differential response of CD4+ V7+ and CD4+ V7- T cells to T cell receptor-dependent signals: CD4+ V7+ T cells are co-stimulation independent and anti-V7 antibody blocks the induction of anergy by bacterial superantigen. European Journal of Immunology , UK, v. 27, n.6, p. 1413-1421, 1997.

• BENICHOU, Gilles ; SOARES, Luis ; FEDOSEYEVA, Eugenia . Indirect T-cell allorecognition: perspectives for peptide-based therapy in transplantation. Immunology Today , USA, v. 18, n.2, p. 67-71, 1997.

• BENICHOU, Gilles ; SOARES, Luis ; FEDOSEYEVA, Eugenia . The influence of two distinct alloresponse pathways on the design of peptide-based strategies for allograft tolerance.. Research in Immunology , França, v. 147, n.6, p. 377-387, 1996.

• KUMAR, Vipin ; SOARES, Luis ; SERCARZ, Eli . Major histocompatibility complex binding affinity of an antigenic determinant is crucial for the differential secretion of interleukin 4/5 or interferon gamma by T cells. . PNAS. Proceedings of the National Academy of Sciences of the United States of America , USA, v. 92, n.21, p. 9510-9514, 1995.

• SOARES, Luis ; MILLER, Alexander ; SERCARZ, Eli . Determinant flanking regions and the design of appropriate vaccines. . Annals of the New York Academy of Sciences , USA, v. 754, p. 48-56, 1995.

• SOARES, Luis ; SERCARZ, Eli ; MILLER, Alexander . Vaccination of the Leishmania major susceptible BALB/c mouse. I. The precise selection of peptide determinant influences CD4+ T cell subset expression. International Immunology , USA, v. 6, n.5, p. 785-794, 1994.

• BARCINSKI, Marcello ; SOARES, Luis ; CHARLAB, Rosane . Granulocyte-macrophage colony-stimulating factor increases the infectivity of Leishmania amazonensis by protecting promastigotes from heat-induced death. Infection and Immunity , USA, v. 60, n.9, p. 3523-3527, 1992.

• SOARES, Luis ; BARCINSKI, Marcello . Differential production of granulocyte-macrophage colony-stimulating factor by macrophages from mice susceptible and resistant to Leishmania mexicana amazonensis.. Journal of Leukocyte Biology , USA, v. 51, n.3, p. 220-224, 1992.

• BARCINSKI, Marcello ; SOARES, Luis ; MAGALHAES, Am . The role of hematopoietic growth factors in the fate of an infection with Leishmania mexicana amazonensis: an attempt at a unifying hypothesis. Memórias do Instituto Oswaldo Cruz , Brasil, v. 83, n.1, p. 1411-1413, 1988.

Projetos de pesquisa

• 2007 - 2010

  Biologia de Sistemas em infecções virais, Descrição: Ferramentas de Bioinformática e Yeast two-hybrids. , Situação: Em andamento; Natureza: Pesquisa. , Alunos envolvidos: Mestrado acadêmico: (1) . , Integrantes: Luis Roberto Benghi Soares - Coordenador., Financiador(es): National Institute Of Health - Cooperação.

• 1998 - 2002

  T cell tolerance (Financiado pelo NIH), Descrição: Signaling T Cell Anergy While the descriptive aspect of anergy has not reached a common consensus, the molecular understanding of anergy is even more hotly debated. The prevalent viewpoint in signaling anergy by APLs is that a partial (suboptimal) is sent through the TCR to initiate an anergy-inducing program. APLs carry point mutations at their TCR contact residues, creating different topologies of peptide-MHC at the TCR interface. It has been proposed that APLs are unable to induce proper conformational changes in the TCR and their fast TCR/MHC dissassociation cannot send an optimal signal for activation but sufficient for induction of anergy. The kinetic proofreading theory proposing that rapid TCR dissociation from APLs leads to incomplete phosphorylation of signaling cascades directly linked to the TCR-CD3 complex and is associated with the formation of an unstable immunological synapse (Kupfer, Heismeyer). APL anergized cells showed poor transmembrane signaling, including partial phosphorylation of the TCR zeta chain, lack of activation of TCR associated ZAP-70, poor phosphorylation of various tyrosine kinases and of the MAPK kinases, ERK1/2 and p38; deficient degradation of phosphorylated IkappaBalpha; increased expression of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) (Sloan-Lancaster, Shaw et al. 1994; Sloan-Lancaster and Allen 1995; Sloan-Lancaster, Steinberg et al. 1996; Mirshahidi, Huang et al. 2001; Mirshahidi, Ferris et al. 2004). These defects in proximal signaling appear to block proliferative responses in these cells. Moreover, the APL-stimulated intracellular Ca+2 induction is both initiated and sustained at lower levels than that stimulated by a strong agonist signal, but resembles that stimulated by a weaker agonist stimulus (Sloan-Lancaster, Steinberg et al. 1996). . , Situação: Concluído; Natureza: Pesquisa. , Alunos envolvidos: Graduação: (0) / Especialização: (0) / Mestrado acadêmico: (0) / Mestrado profissional: (0) / Doutorado: (0) . , Integrantes: Luis Roberto Benghi Soares - Coordenador., Financiador(es): National Institute Of Health - Auxílio financeiro., Número de produções C, T & A: 2

• 1998 - Atual

  T cell tolerance in type I (autoimmune diabetes) (Financiado pelo NIH), Descrição: Specific Aims: Studies proposed in this grant application intend to identify the mechanisms of effect that allow systemic administration of anti-CD3 antibody to block progression to overt diabetes in recent onset hyperglycemic NOD mice, and returns these mice to persistent euglycemia. These studies will integrate novel techniques in proteomics (cell lysate arrays and intracellular phospho-epitope analysis) and conventional proteomic assays (ELISA and histopathology), with state of the art cDNA microarray analysis of islet tissues and peripheral lymphoid tissues in treated versus untreated control mice to characterize the gene expression profile of these tissues following therapy in order to link the observed gene expression profile to proteins that effect, or result from, this therapy. Characterization and analysis of gene and proteome expression following successful anti-CD3 therapy of NOD mice should provide important insights into mechanism of effect and may provide additional or alternative targets for future therapies. The hypothesis being tested is the following: Two major phenomenon occur following systemic anti-CD3 therapy of recently hyperglycemic NOD mice; (1) a change in the immune response profile of the pathogenic T cells that halts the autoimmune destruction of beta cells occurs, and (2) beta cell regeneration (wound healing) is a consequence of this change in immune response. The following five specific aims have been developed to examine this hypothesis: (1) By analysis of gene expression patterns in islet infiltrating as well as peripheral T lymphocytes following successful anti-CD3 therapy of recent onset hyperglycemic NOD mice, it will be possible to characterize pathways of immune response that have been changed by therapy. (2) By similar analysis of the expressed genome of pancreatic beta cells from untreated or treated NOD mice versus non-inflamed NOD.B10 islets, a gene expression profile of regenerating islets cells can be obta. , Situação: Em andamento; Natureza: Pesquisa. , Alunos envolvidos: Graduação: (1) / Especialização: (0) / Mestrado acadêmico: (0) / Mestrado profissional: (0) / Doutorado: (1) . , Integrantes: Luis Roberto Benghi Soares - Coordenador., Financiador(es): National Institute Of Health - Auxílio financeiro.