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12 results on '"Silva, Henrique"'

1. Comparison of rheumatoid arthritis composite disease activity indices and residual activity in a Brazilian multicenter study- REAL study

Author

Santos, Isabela Araújo, primary, Donizeti Ribeiro de Oliveira, Renê, additional, Couto Luna Almeida, Sergio, additional, Vargas-Santos, Ana Beatriz, additional, Balbino Chaves Amorim, Rodrigo, additional, Monteiro Gomides, Ana Paula, additional, de Albuquerque, Cleandro Pires, additional, Barros Bertolo, Manoel, additional, Brandão Resende Guimarães, Maria Fernanda, additional, da Costa Pinto, Maria Raquel, additional, Gomes Resende, Gustavo, additional, Dalva Neubarth Giorgi, Rina, additional, de Carvalho Saciloto, Nathalia, additional, Radominski, Sebastião Cezar, additional, Borghi, Fernanda Maria, additional, Rossi Bonfiglioli, Karina, additional, Carrico da Silva, Henrique, additional, de Fatima L. da Cunha Sauma, Maria, additional, Alves Pereira, Ivanio, additional, Werner de Castro, Glaucio Ricardo, additional, Viegas Brenol, Claiton, additional, Machado Xavier, Ricardo, additional, Maria Henrique Mota, Licia, additional, Louzada-Junior, Paulo, additional, and da Rocha Castelar-Pinheiro, Geraldo, additional

Published
2022
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2. Discordance between the patient’s and physician’s global assessment in rheumatoid arthritis: Data from the REAL study—Brazil

Author

Guimarães, Maria Fernanda Brandão Resende, primary, Pinto, Maria Raquel da Costa, additional, Resende, Gustavo Gomes, additional, Machado, Carla Jorge, additional, Vargas-Santos, Ana Beatriz, additional, Amorim, Rodrigo Balbino Chaves, additional, Gomides, Ana Paula Monteiro, additional, Albuquerque, Cleandro Pires de, additional, Bértolo, Manoel Barros, additional, Júnior, Paulo Louzada, additional, Santos, Isabela Araújo, additional, Giorgi, Rina Dalva Neubarth, additional, Saciloto, Nathalia de Carvalho, additional, Radominski, Sebastião Cezar, additional, Borghi, Fernanda Maria, additional, Bonfiglioli, Karina Rossi, additional, Silva, Henrique Carriço da, additional, Sauma, Maria de Fátima L. da Cunha, additional, Sauma, Marcel Lobato, additional, Medeiros, Júlia Brito de, additional, Pereira, Ivânio Alves, additional, Castro, Gláucio Ricardo Werner de, additional, Brenol, Claiton Viegas, additional, Xavier, Ricardo Machado, additional, Mota, Licia Maria Henrique, additional, and Castelar-Pinheiro, Geraldo da Rocha, additional

Published
2020
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3. Correction: Causes of synthetic disease-modifying drug discontinuation in rheumatoid arthritis: Data from a large real-life cohort

Author

Gomides, Ana Paula Monteiro, primary, de Albuquerque, Cleandro Pires, additional, Santos, Ana Beatriz Vargas, additional, Amorim, Rodrigo Balbino Chaves, additional, Bértolo, Manoel Barros, additional, Júnior, Paulo Louzada, additional, Santos, Isabela Araújo, additional, Giorgi, Rina Dalva Neubarth, additional, Sacilotto, Nathalia de Carvalho, additional, Radominski, Sebastião Cezar, additional, Borghi, Fernanda Maria, additional, Guimarães, Maria Fernanda B. Resende, additional, Pinto, Maria Raquel da Costa, additional, Resende, Gustavo Gomes, additional, Bonfiglioli, Karina Rossi, additional, Silva, Henrique Carriço da, additional, Sauma, Maria de Fátima Lobato da Cunha, additional, Sauma, Marcel Lobato, additional, de Medeiros, Júlia Brito, additional, Pereira, Ivânio Alves, additional, de Castro, Gláucio Ricardo Werner, additional, Brenol, Claiton Viegas, additional, Xavier, Ricardo Machado, additional, da Mota, Licia Maria Henrique, additional, and Pinheiro, Geraldo da Rocha Castelar, additional

Published
2019
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5. Causes of synthetic disease-modifying drug discontinuation in rheumatoid arthritis: Data from a large real-life cohort

Author

Gomides, Ana Paula Monteiro, primary, de Albuquerque, Cleandro Pires, additional, Santos, Ana Beatriz Vargas, additional, Amorim, Rodrigo Balbino Chaves, additional, Bértolo, Manoel Barros, additional, Júnior, Paulo Louzada, additional, Santos, Isabela Araújo, additional, Giorgi, Rina Dalva Neubarth, additional, Sacilotto, Nathalia de Carvalho, additional, Radominski, Sebastião Cezar, additional, Borghi, Fernanda Maria, additional, Guimarães, Maria Fernanda B. Resende, additional, Pinto, Maria Raquel da Costa, additional, Resende, Gustavo Gomes, additional, Bonfiglioli, Karina Rossi, additional, Silva, Henrique Carriço da, additional, Sauma, Maria de Fátima Lobato da Cunha, additional, Sauma, Marcel Lobato, additional, de Medeiros, Júlia Brito, additional, Pereira, Ivânio Alves, additional, de Castro, Gláucio Ricardo Wernwer, additional, Brenol, Claiton Viegas, additional, Xavier, Ricardo Machado, additional, da Mota, Licia Maria Henrique, additional, and Pinheiro, Geraldo da Rocha Castelar, additional

Published
2019
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7. Oral Outbreak of Chagas Disease in Santa Catarina, Brazil: Experimental Evaluation of a Patient’s Strain

Author

Domingues, Carolina S., primary, Hardoim, Daiana J., additional, Souza, Celeste S. F., additional, Cardoso, Flávia O., additional, Mendes, Verônica G., additional, Previtalli-Silva, Henrique, additional, Abreu-Silva, Ana L., additional, Pelajo-Machado, Marcelo, additional, Gonçalves da Costa, Sylvio Celso, additional, and Calabrese, Kátia S., additional

Published
2015
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8. CD28 deficiency leads to accumulation of germinal-center independent IgM+ experienced B cells and to production of protective IgM during experimental malaria.

Author

Borges da Silva, Henrique, Machado de Salles, Érika, Lima-Mauro, Eliana Faquim, Sardinha, Luiz Roberto, Álvarez, José Maria, and D’Império Lima, Maria Regina

Subjects
*IMMUNOGLOBULIN M, *MALARIA prevention, *B cells, *IMMUNE response, *CD28 antigen, *AUTOANTIGENS, *PHYSIOLOGY
Abstract

Protective immunity to blood-stage malaria is attributed to Plasmodium-specific IgG and effector-memory T helper 1 (Th1) cells. However, mice lacking the costimulatory receptor CD28 (CD28KO) maintain chronic parasitemia at low levels and do not succumb to infection, suggesting that other immune responses contribute to parasite control. We report here that CD28KO mice develop long-lasting non-sterile immunity and survive lethal parasite challenge. This protection correlated with a progressive increase of anti-parasite IgM serum levels during chronic infection. Serum IgM from chronically infected CD28KO mice recognize erythrocytes infected with mature parasites, and effectively control Plasmodium infection by promoting parasite lysis and uptake. These antibodies also recognize autoantigens and antigens from other pathogens. Chronically infected CD28KO mice have high numbers of IgM+ plasmocytes and experienced B cells, exhibiting a germinal-center independent Fas+GL7-CD38+CD73- phenotype. These cells are also present in chronically infected C57BL/6 mice although in lower numbers. Finally, IgM+ experienced B cells from cured C57BL/6 and CD28KO mice proliferate and produce anti-parasite IgM in response to infected erythrocytes. This study demonstrates that CD28 deficiency results in the generation of germinal-center independent IgM+ experienced B cells and the production of protective IgM during experimental malaria, providing evidence for an additional mechanism by which the immune system controls Plasmodium infection. [ABSTRACT FROM AUTHOR]

Published
2018
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9. Behavioral Phenotyping of Parkin-Deficient Mice: Looking for Early Preclinical Features of Parkinson's Disease

Author

Rial, Daniel, primary, Castro, Adalberto A., additional, Machado, Nuno, additional, Garção, Pedro, additional, Gonçalves, Francisco Q., additional, Silva, Henrique B., additional, Tomé, Ângelo R., additional, Köfalvi, Attila, additional, Corti, Olga, additional, Raisman-Vozari, Rita, additional, Cunha, Rodrigo A., additional, and Prediger, Rui D., additional

Published
2014
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11. Liver Accumulation of Plasmodium chabaudi-Infected Red Blood Cells and Modulation of Regulatory T Cell and Dendritic Cell Responses.

Author

Medeiros, Márcia M., Silva, Henrique B. da, Reis, Aramys S., Barboza, Renato, Thompson, Joanne, Lima, Maria Regina D'Império, Marinho, Cláudio R. F., and Tadokoro, Carlos E.

Subjects
*DENDRITIC cells, *T cells, *ERYTHROCYTES, *IMMUNE system, *BIOACCUMULATION, *PLASMODIUM
Abstract

It is postulated that accumulation of malaria-infected Red Blood Cells (iRBCs) in the liver could be a parasitic escape mechanism against full destruction by the host immune system. Therefore, we evaluated the in vivo mechanism of this accumulation and its potential immunological consequences. A massive liver accumulation of P. c. chabaudi AS-iRBCs (Pc-iRBCs) was observed by intravital microscopy along with an over expression of ICAM-1 on day 7 of the infection, as measured by qRT-PCR. Phenotypic changes were also observed in regulatory T cells (Tregs) and dendritic cells (DCs) that were isolated from infected livers, which indicate a functional role for Tregs in the regulation of the liver inflammatory immune response. In fact, the suppressive function of liver-Tregs was in vitro tested, which demonstrated the capacity of these cells to suppress naive T cell activation to the same extent as that observed for spleen-Tregs. On the other hand, it is already known that CD4+ T cells isolated from spleens of protozoan parasite-infected mice are refractory to proliferate in vivo. In our experiments, we observed a similar lack of in vitro proliferative capacity in liver CD4+ T cells that were isolated on day 7 of infection. It is also known that nitric oxide and IL-10 are partially involved in acute phase immunosuppression; we found high expression levels of IL-10 and iNOS mRNA in day 7-infected livers, which indicates a possible role for these molecules in the observed immune suppression. Taken together, these results indicate that malaria parasite accumulation within the liver could be an escape mechanism to avoid sterile immunity sponsored by a tolerogenic environment. [ABSTRACT FROM AUTHOR]

Published
2013
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