Advanced search
Start date
Betweenand

The involvement of the Major Histocompatibility Complex Class I molecules in the astrocytic reactivity after sciatic nerve transection

Grant number: 12/20456-6
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): December 01, 2012
Effective date (End): November 30, 2013
Field of knowledge:Biological Sciences - Immunology
Principal Investigator:André Luis Bombeiro
Grantee:Sérgio Luiz Oliveira Nunes
Home Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil

Abstract

A growing number of studies has demonstrated the involvement of the major histocompatibility complex class I (MHC-I) molecules in distinct processes of antigen presentation to the cytotoxic T cells (T CD8) of the immune system. Although the expression of MHC-I molecules by neurons is low in basal conditions, it has been demonstrated that these cells are able to significantly enhance the expression of MHC-I under injury as well as during certain stages of the embryonic development. Besides the classic receptor of MHC-I is present on T cells (TCR), there are also other molecules that bind to MHC-I, among them the Paired immunoglobulin-like receptor B (PIR-B), with inhibitory activity, which is present in different immune cells as well as in the projections of neurons under injury or during the embryonic development. Some peripheral nerve injuries can trigger retrograde cellular responses in the spinal cord, such as chromatolysis of axotomized neurons accompanied by an increased astrocytic reactivity, and in these cases, astrocytes may act in the synapse striping of those damaged neurons, which can also overexpress MHC-I. It is worth to mention that peripheral lesions do not evoke inflammation in the spinal cord, as so the MHC-I molecules expressed in sites that are distant from the lesion do not act in the process of immune surveillance. In view of the above, this project proposes to assess the involvement of MHC-I molecules and their ligand PIR-B in the process of astrocytic reactivity in the spinal cord of mice that were submitted to the sciatic nerve transection.

Scientific publications (4)
(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)
ARAUJO, MARTA ROCHA; KYRYLENKO, SERGIY; SPEJO, ALINE BARROSO; CASTRO, MATEUS VIDIGAL; FERREIRA JUNIOR, RUI SEABRA; BARRAVIERA, BENEDITO; RODRIGUES OLIVEIRA, ALEXANDRE LEITE. Transgenic human embryonic stem cells overexpressing FGF2 stimulate neuroprotection following spinal cord ventral root avulsion. Experimental Neurology, v. 294, p. 45-57, AUG 2017. Web of Science Citations: 7.
BISCOLA, NATALIA PERUSSI; CARTAROZZI, LUCIANA POLITTI; ULIAN-BENITEZ, SUZANA; BARBIZAN, ROBERTA; CASTRO, MATEUS VIDIGAL; SPEJO, ALINE BARROSO; FERREIRA, JR., RUI SEABRA; BARRAVIERA, BENEDITO; RODRIGUES OLIVEIRA, ALEXANDRE LEITE. Multiple uses of fibrin sealant for nervous system treatment following injury and disease. Journal of Venomous Animals and Toxins including Tropical Diseases, v. 23, n. 1 MAR 14 2017. Web of Science Citations: 19.
NATALIA PERUSSI BISCOLA; LUCIANA POLITTI CARTAROZZI; SUZANA ULIAN-BENITEZ; ROBERTA BARBIZAN; MATEUS VIDIGAL CASTRO; ALINE BARROSO SPEJO; RUI SEABRA FERREIRA JR.; BENEDITO BARRAVIERA; ALEXANDRE LEITE RODRIGUES OLIVEIRA. Multiple uses of fibrin sealant for nervous system treatment following injury and disease. Journal of Venomous Animals and Toxins including Tropical Diseases, v. 23, p. -, 2017.
BOMBEIRO, ANDRE L.; SANTINI, JULIO C.; THOME, RODOLFO; FERREIRA, ELISANGELA R. L.; NUNES, SERGIO L. O.; MOREIRA, BARBARA M.; BONET, IVAN J. M.; SARTORI, CESAR R.; VERINAUD, LIANA; OLIVEIRA, ALEXANDRE L. R. Enhanced Immune Response in Immunodeficient Mice Improves Peripheral Nerve Regeneration Following Axotomy. FRONTIERS IN CELLULAR NEUROSCIENCE, v. 10, JUN 14 2016. Web of Science Citations: 14.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.