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6 results on '"Moctezuma, J. F."'

1. FRI0546 GENDER DIFFERENCES OF RHEUMATIC DISEASES IN MEXICAN POPULATION: DATA FROM THE MEXICAN BIOLOGICS REGISTRY

Author

Rivera Teran, V., primary, Alpizar-Rodriguez, D., additional, Sicsik, S., additional, Irazoque-Palazuelos, F., additional, Miranda, D., additional, Vega-Morales, D., additional, Casasola, J. C., additional, Carrilo, S., additional, Castillo, A., additional, Duran Barragan, S., additional, Muñoz, O., additional, Paz, A., additional, Peña, A., additional, Torres, A., additional, Xibille Friedmann, D. X., additional, Ramos, A., additional, Moctezuma, J. F., additional, Aceves, F., additional, Torres, E., additional, Santana, N., additional, Vazquez, M., additional, Zamora, E., additional, Guerrero, F., additional, Zepeda, C., additional, Rivera, M., additional, Alvarado, K., additional, and Pacheco Tena, C. F., additional

Published
2020
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2. AB1229 SAFETY OF BIOSIMILAR ETANERCEPT IN THE TREATMENT OF RHEUMATIC DISEASES: DATA FROM THE MEXICAN ADVERSE EVENTS REGISTRY (BIOBADAMEX)

Author

Rivera Teran, V., primary, Pérez Rodríguez, M., additional, Alpizar-Rodriguez, D., additional, Irazoque-Palazuelos, F., additional, Carrilo, S., additional, Sicsik, S., additional, Vega-Morales, D., additional, Miranda, D., additional, Castillo, A., additional, Casasola, J. C., additional, Pacheco Tena, C. F., additional, Moctezuma, J. F., additional, Aceves, F., additional, Paz, A., additional, Duran Barragan, S., additional, Barile, L., additional, Santana, N., additional, and Xibille Friedmann, D. X., additional

Published
2020
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4. Preferential Binding to Elk-1 by SLE-Associated IL10 Risk Allele Upregulates IL10 Expression

Author

Sakurai, D., Zhao, J., Deng, Y., Kelly, J. A., Brown, E. E., Harley, J. B., Bae, S. C., Alarcón-Riquelme, M. E., Edberg, J. C., Kimberly, R. P., Ramsey-Goldman, R., Caeiro, F., Soriano, E. R., Bertoli, A., Prigione, C., Ramos, F. A., Romero, E. J., Tsao, B. P., Chen, W., Truedsson, L., Yu, C. Y., Migliarese, S., García, M. A., Marcos, J. C., Eimon, A., Sánchez-Román, J., Battagliotti, C. G., Kaufman, K. M., Vyse, T. J., Jacob, C. O., Gaffney, P. M., Sebastiani, G. D., Ramón, Enrique de, Hahn, B. H., Song, Y. W., Grossman, J. M., Sivils, K. M., James, J. A., Kamen, D. L., Gilkeson, G. S., Niewold, T. B., D'Alfonso, Sandra, Merrill, J. T., Martín, J., Scofield, R. H., Chang, D. M., Criswell, L. A., Langefeld, C. D., Stevens, A. M., Cantor, R. M., Frostegård, Johan, Boackle, S. A., Kim, J. H., Choi, J., Pons-Estel, B. A., Freedman, Barry I., Sabio, José Mario, Anaya, J. M., Ortego-Centeno, N., Callejas-Rubio, J. L., González-Escribano, María Francisca, Buchanan, G., Graf, C. E., Paira, S., Galeazzi, M., Witte, Torsten, Lauwerys, B. R., Endreffy, E., Kovács, L., Vasconcelos, C., Silva, B. M. da, Scherbarth, H. R., Catoggio, L. J., Manni, J., Caprarulo, C., Guillerón, C., Marino, P. C., Motta, E. L., Gamron, S., Drenkard, C., Menso, E., Allievi, A., Roverano, S., Tate, G. A., Bertero, E., Presas, J. L., Navarro, S. M., Parque, S., Grimaudo, S., Palatnik, S. A., Abdala, M., Acevedo, E., Bearzotti, M., Santos, C. D., Alvarellos, A., Berbotto, G. A., Jorfen, M., Marcos, A. I., Perandones, C. E., Cucho, M., Torre, I. G. de la, Ríos, M. C., Moctezuma, J. F., Ceceña, M. M., Petri, M. A., Vilá, Luis M., Reveille, J. D., Alarcón, G. S., Sakurai, D., Zhao, J., Deng, Y., Kelly, J. A., Brown, E. E., Harley, J. B., Bae, S. C., Alarcón-Riquelme, M. E., Edberg, J. C., Kimberly, R. P., Ramsey-Goldman, R., Caeiro, F., Soriano, E. R., Bertoli, A., Prigione, C., Ramos, F. A., Romero, E. J., Tsao, B. P., Chen, W., Truedsson, L., Yu, C. Y., Migliarese, S., García, M. A., Marcos, J. C., Eimon, A., Sánchez-Román, J., Battagliotti, C. G., Kaufman, K. M., Vyse, T. J., Jacob, C. O., Gaffney, P. M., Sebastiani, G. D., Ramón, Enrique de, Hahn, B. H., Song, Y. W., Grossman, J. M., Sivils, K. M., James, J. A., Kamen, D. L., Gilkeson, G. S., Niewold, T. B., D'Alfonso, Sandra, Merrill, J. T., Martín, J., Scofield, R. H., Chang, D. M., Criswell, L. A., Langefeld, C. D., Stevens, A. M., Cantor, R. M., Frostegård, Johan, Boackle, S. A., Kim, J. H., Choi, J., Pons-Estel, B. A., Freedman, Barry I., Sabio, José Mario, Anaya, J. M., Ortego-Centeno, N., Callejas-Rubio, J. L., González-Escribano, María Francisca, Buchanan, G., Graf, C. E., Paira, S., Galeazzi, M., Witte, Torsten, Lauwerys, B. R., Endreffy, E., Kovács, L., Vasconcelos, C., Silva, B. M. da, Scherbarth, H. R., Catoggio, L. J., Manni, J., Caprarulo, C., Guillerón, C., Marino, P. C., Motta, E. L., Gamron, S., Drenkard, C., Menso, E., Allievi, A., Roverano, S., Tate, G. A., Bertero, E., Presas, J. L., Navarro, S. M., Parque, S., Grimaudo, S., Palatnik, S. A., Abdala, M., Acevedo, E., Bearzotti, M., Santos, C. D., Alvarellos, A., Berbotto, G. A., Jorfen, M., Marcos, A. I., Perandones, C. E., Cucho, M., Torre, I. G. de la, Ríos, M. C., Moctezuma, J. F., Ceceña, M. M., Petri, M. A., Vilá, Luis M., Reveille, J. D., and Alarcón, G. S.

Abstract

Immunoregulatory cytokine interleukin-10 (IL-10) is elevated in sera from patients with systemic lupus erythematosus (SLE) correlating with disease activity. The established association of IL10 with SLE and other autoimmune diseases led us to fine map causal variant(s) and to explore underlying mechanisms. We assessed 19 tag SNPs, covering the IL10 gene cluster including IL19, IL20 and IL24, for association with SLE in 15,533 case and control subjects from four ancestries. The previously reported IL10 variant, rs3024505 located at 1 kb downstream of IL10, exhibited the strongest association signal and was confirmed for association with SLE in European American (EA) (P = 2.7×10-8, OR = 1.30), but not in non-EA ancestries. SNP imputation conducted in EA dataset identified three additional SLE-associated SNPs tagged by rs3024505 (rs3122605, rs3024493 and rs3024495 located at 9.2 kb upstream, intron 3 and 4 of IL10, respectively), and SLE-risk alleles of these SNPs were dose-dependently associated with elevated levels of IL10 mRNA in PBMCs and circulating IL-10 protein in SLE patients and controls. Using nuclear extracts of peripheral blood cells from SLE patients for electrophoretic mobility shift assays, we identified specific binding of transcription factor Elk-1 to oligodeoxynucleotides containing the risk (G) allele of rs3122605, suggesting rs3122605 as the most likely causal variant regulating IL10 expression. Elk-1 is known to be activated by phosphorylation and nuclear localization to induce transcription. Of interest, phosphorylated Elk-1 (p-Elk-1) detected only in nuclear extracts of SLE PBMCs appeared to increase with disease activity. Co-expression levels of p-Elk-1 and IL-10 were elevated in SLE T, B cells and monocytes, associated with increased disease activity in SLE B cells, and were best downregulated by ERK inhibitor. Taken together, our data suggest that preferential binding of activated Elk-1 to the IL10 rs3122605-G allele upregulates IL10 expressio

Published
2013

5. THU0208 Comparative, Randomized, Simple Blind to Evaluate Efficacy and Safety of Infinitam® (Etanercept), Associated with Methotrexate Compared with Enbrel® (Etanercept) Associated with Methotrexate in Patients with Modeate and Severe Rheumatoid Arthritis

Author

Moctezuma, J. F., primary, Martinez, A., additional, Enkerlin, H., additional, Garcia, C., additional, Chavez, B., additional, Salazar-Teran, N., additional, Molina, A., additional, and Revilla, J., additional

Published
2013
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6. Anti-CD43 and anti-galectin-1 autoantibodies in patients with systemic lupus erythematosus.

Author

Montiel JL, Monsiváis-Urenda A, Figueroa-Vega N, Moctezuma JF, Burgos-Vargas R, González-Amaro R, and Rosenstein Y

Subjects
Adolescent, Adult, Age Factors, Biomarkers blood, Case-Control Studies, Enzyme-Linked Immunosorbent Assay, Female, Galectin 1 blood, Humans, Leukosialin blood, Lupus Erythematosus, Systemic diagnosis, Male, Prognosis, Reference Values, Risk Assessment, Severity of Illness Index, Sex Factors, Young Adult, Autoantibodies blood, Galectin 1 immunology, Leukosialin immunology, Lupus Erythematosus, Systemic immunology
Abstract

Objectives: Systemic lupus erythematosus (SLE) is characterized by the production of multiple autoantibodies and also by T-cell dysfunction. CD43 is expressed by most immune cells, is involved in lymphocyte adhesion and activation, and interacts with galectin-1 (Gal-1). The aim of this work was to evaluate the plasma levels of autoantibodies against CD43 and Gal-1 as well as the levels of soluble Gal-1 in SLE Mexican mestizo patients, with the aim of establishing a correlation between these parameters and the clinical profile., Methods: Serum levels of immunoglobulin (Ig)G autoantibodies against CD43 and Gal-1 and levels of soluble Gal-1 were measured by enzyme-linked immunosorbent assay (ELISA) in 55 patients with SLE and 71 healthy controls., Results: We found significantly enhanced titres of anti-CD43 and anti-Gal-1 antibodies in sera from SLE patients compared to controls. In addition, the serum levels of Gal-1 were significantly higher in SLE patients than in healthy individuals. However, we could detect no correlation of these parameters with disease activity [using the Mexican Systemic Lupus Erythematosus Disease Activity Index (MEX-SLEDAI)], age, or a variety of different clinical or laboratory features. Similarly, no significant correlation with immunosuppressive or glucocorticoid therapy was observed. By contrast, a significant association was found between anti-CD43 titres and time of disease evolution, complement levels, and the presence of anti-Gal-1 antibodies., Conclusions: As CD43 and Gal-1 participate in modulating the immune system, we suggest that the presence of autoantibodies against these molecules may contribute to the immune deregulation observed in SLE.

Published
2010
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