dc.creator | Quiroga, María Florencia | |
dc.creator | Jurado, Javier Oscar | |
dc.creator | Martínez, Gustavo Javier | |
dc.creator | Pasquinelli, Virginia | |
dc.creator | Musella, Rosa María | |
dc.creator | Abbate, Pablo Eduardo | |
dc.creator | Issekutz, Andrew C. | |
dc.creator | Bracco, María Marta | |
dc.creator | Malbrán, Alejandro | |
dc.creator | Sieling, Peter Allan | |
dc.creator | Chuluyan, Hector Eduardo | |
dc.creator | García, Verónica Edith | |
dc.date.accessioned | 2017-07-13T00:04:36Z | |
dc.date.available | 2017-07-13T00:04:36Z | |
dc.date.created | 2017-07-13T00:04:36Z | |
dc.date.issued | 2007-11 | |
dc.identifier | Quiroga, María Florencia; Jurado, Javier Oscar; Martínez, Gustavo Javier; Pasquinelli, Virginia; Musella, Rosa María; et al.; (última autoría compartida) Cross-talk between CD31 and the signaling lymphocytic activation molecule-associated protein during interferon- gamma production against Mycobacterium tuberculosis.; Oxford University Press; Journal Of Infectious Diseases; 196; 9; 11-2007; 1369-1378 | |
dc.identifier | 0022-1899 | |
dc.identifier | http://hdl.handle.net/11336/20325 | |
dc.identifier | CONICET Digital | |
dc.identifier | CONICET | |
dc.description.abstract | Effective host defense against tuberculosis requires Th1 cytokine responses. We studied the regulation of interferon (IFN)-γ production during tuberculosis by investigating the role of CD31, a receptor that attenuates T cell receptor signals. After antigen stimulation, CD3+CD31+ blood lymphocytes decreased in healthy donors and in tuberculosis patients with robust Th1 responses to Mycobacterium tuberculosis and IFN-γ was secreted only by CD31- T cells. In contrast, in patients with weak Th1 cytokine responses to M. tuberculosis, the level of CD3+CD31+ lymphocytes was increased and IFN-γ production was low. Furthermore, the inverse relationship between CD31 expression and IFN-γ production was in contrast to signaling lymphocytic activation molecule (SLAM) expression, an IFN-γ inducer in tuberculosis. Interestingly, CD31 bound to SLAM-associated protein (SAP), an IFN-γ inhibitor in tuberculosis, and when CD31 and SAP were coexpressed in lymphocytes, their association inhibited the IFN-γ response to M. tuberculosis. Thus, CD31, when binding to SAP, interferes with Th1 responses, suggesting that CD31 has a key regulatory role in the signaling pathway(s) leading to the IFN-γ response to M. tuberculosis. | |
dc.language | eng | |
dc.publisher | Oxford University Press | |
dc.relation | info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/jid/article-lookup/doi/10.1086/522522 | |
dc.relation | info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1086/522522 | |
dc.rights | https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | Cytokines | |
dc.subject | Signal Transduction | |
dc.subject | Antigens | |
dc.subject | Tuberculosis | |
dc.subject | Molecule | |
dc.subject | Donors | |
dc.title | (última autoría compartida) Cross-talk between CD31 and the signaling lymphocytic activation molecule-associated protein during interferon- gamma production against Mycobacterium tuberculosis. | |
dc.type | info:eu-repo/semantics/article | |
dc.type | info:ar-repo/semantics/artículo | |
dc.type | info:eu-repo/semantics/publishedVersion | |