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Effect of BAY 41-2272 in human T lymphocytes.

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Marina Uchôa Wall Barbosa de Carvalho
Total Authors: 1
Document type: Doctoral Thesis
Press: São Paulo.
Institution: Universidade de São Paulo (USP). Instituto de Ciências Biomédicas
Defense date:
Examining board members:
Antonio Condino Neto; Edson Antunes; Sonia Jancar Negro; Edgar Borges de Oliveira Junior; Alexandre Alarcon Steiner
Advisor: Antonio Condino Neto

In this work, we evaluated the potential of BAY 41-2272 and its pathway as a tool for modulating lymphocyte function. For this, we performed pharmacological treatments with BAY 41-2272, evaluating the production of cytokines and observed that this drug, as a direct activator, does not induce production of IFN, IL-4 e IL-10. However, pre-treatment for 24 hours with BAY 41-2272 and subsequente activation with PMA showed that this drug has an inhibitory effect on cytokine production. Thus, we evaluated if this drug would be able to activate these cells through the CD69 expression. We saw that alone, BAY 41-2272 was not able to increase CD69 expression, however, pre-treatment inhibited activation of CD4 T lymphocytes. Then, we evaluated if this chemical compound would be able to inhibite the expression of transcription factors FOXP3, RORT, Tbet and GATA3. We have seen that BAY 41-2272 did not induce expression of these transcription factors and pretreatment with this drug did not alter expression of FOXP3, RORT and GATA3, but inhibited Tbet expression. We also observed that pre-treatment with BAY 41-2272 inhibited lymphoproliferation. These results suggest that BAY 41-2272 and its pathway have an inhibitory profile on CD4 T lymphocytes and can potentially be used as an immunomodulator in patients with impaired imune system and lymphoproliferative syndromes. (AU)

FAPESP's process: 13/11097-5 - Efect of BAY 41 22-72, soluble guanylate cyclase agonist, in human T cells and Jurkat cells.
Grantee:Marina Uchôa Wall Barbosa de Carvalho
Support type: Scholarships in Brazil - Doctorate