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Evaluation of B-1 cell precursor population in the aging: possible relation with hyperproliferatives diseases

Grant number: 17/11725-7
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date: September 01, 2017
End date: December 31, 2019
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Ana Flavia Popi
Grantee:Olívia Fonseca Souza
Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Hyperproliferative diseases, such as Chronic Lymphocytic Leukemia (CLL) and Systemic Lupus Erythematosus (SLE) are possibly related to some disturb in the apoptosis pathway, specifically in B-1a cells (CD5+). These problems result in the accumulation of B-1a cells in lymphoid organs, bone marrow or periphery, as observed in experimental models with old animals. Furthermore, it is known that aging increases B-1 cell population, although it is not yet elucidated if this happens due to self-renewal of mature cells or reactivation of the precursor cell. Based on this, this project aims to investigate parameters of the clonal expansion and/or hyperplasia of the B-1 bone-marrow-derived precursors. The main purpose is to identify possible alterations in the B-1 precursor cell that could be involved in the beginning of these hyperproliferative pathologies, with neoplastic or autoimmune basis. (AU)

News published in Agência FAPESP Newsletter about the scholarship:
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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
SOUZA, OLIVIA F.; DE OLIVEIRA, VIVIAN C.; RODRIGUES, GABRIEL J. F.; COSTA, LUCAS V. S.; CORADO, FERNANDA; POPI, ANA F.. Age-related accumulation of B-1 cell progenitors in mice reflects changes in miR15a/16-1 expression and radioresistance capacity. EXPERIMENTAL HEMATOLOGY & ONCOLOGY, v. 12, n. 1, p. 6-pg., . (17/24451-2, 19/27009-4, 17/11725-7, 21/05377-1)