M
Maria L. Espejo
Researcher at University of California, Los Angeles
Publications - 10
Citations - 645
Maria L. Espejo is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Transplantation & Chemokine. The author has an hindex of 7, co-authored 10 publications receiving 628 citations.
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Journal ArticleDOI
Humoral rejection in cardiac transplantation: risk factors, hemodynamic consequences and relationship to transplant coronary artery disease.
Paul J Michaels,Maria L. Espejo,Jon A. Kobashigawa,Juan C. Alejos,C. Burch,Takemoto S,Elaine F. Reed,Michael C. Fishbein +7 more
TL;DR: Humoral rejection is a clinicopathologic entity with a high incidence in women and is associated with acute hemodynamic compromise, accelerated transplant coronary artery disease and death.
Journal ArticleDOI
Early and late chemokine production correlates with cellular recruitment in cardiac allograft vasculopathy.
James Yun,Michael P. Fischbein,Hillel Laks,Michael C. Fishbein,Maria L. Espejo,Kamyar Ebrahimi,Yoshihito Irie,Judith A. Berliner,Abbas Ardehali +8 more
TL;DR: A dual pattern of chemokine induction correlating with intragraft mononuclear cell recruitment, associated with ischemia-reperfusion and CAV development is demonstrated.
Journal ArticleDOI
Rantes production during development of cardiac allograft vasculopathy.
James Yun,Michael P. Fischbein,Hillel Laks,Yoshihito Irie,Maria L. Espejo,Michael C. Fishbein,Judith A. Berliner,Abbas Ardehali +7 more
TL;DR: Evidence is presented that other cell types in addition to CD4+, CD8+ T lymphocytes, and CD11b+ macrophages contribute significantly to RANTES production in CAV.
Journal ArticleDOI
Incidence of acute cellular rejection and non-cellular rejection in cardiac transplantation
TL;DR: The incidence of noncellular rejection in cardiac transplant recipients has remained unchanged through the 1990s despite improved immunosuppressive therapies, which have significantly decreased the incidence of acute cellular rejection.
Journal ArticleDOI
CD8+ lymphocytes augment chronic rejection in a MHC class II mismatched model.
Michael P. Fischbein,James Yun,Hillel Laks,Yoshihito Irie,Michael C. Fishbein,Maria L. Espejo,Benjamin Bonavida,Abbas Ardehali +7 more
TL;DR: In this MHC class II mismatched murine model, CAV is a T lymphocyte dependent event, and absolutely contingent on the presence of CD4+ lymphocytes, and both CD4 and CD8- lymphocytes contribute to CAV development via secretion of IFN-&ggr;, a known mediator of CAV in this model.