Day 1 :
National Polytechnic Institute, Mexico
Jose L Reyes has completed his MD degree from National University of Mexico (1964). He was a Pediatric Nephrologist in Hospital Infantil de Mexico Federico Gomez (1969), Research fellow in Children’s Hospital of Los Angeles CA, USA. He obtained his PhD degree from Center for Research and Advanced Studies, National Polytechnic Institute, Mexico (1977). He is currently a full Professor at National Polytechnic Institute, Mexico and former Head of the Department of Physiology, Biophysics and Neurosciences. He has been an Invited Professor in the University of Lausanne, Switzerland, 1983-1984, Université de Paris VI, Albert Einstein College of Medicine, USA, New York Medical College, USA, Université de Paris, France, Université de Nice, France and Cambridge University, England. He also has 135 publications.
Diabetes is one of the main causes of renal failure all over the world. The mechanisms initiating diabetic nephropathy have been only partially studied. We analyzed the damage induced by diabetes on the intercellular renal junctions since information on this issue is relevant. Glucose is filtered in the kidney at the glomeruli and is reabsorbed at the proximal tubule. In the absorption of glucose participates SGLT1 and 2, located at the apical brush border and GLUT1 and 2, located at the basolateral membrane of the proximal tubular cells. We explored differentially alterations in the glomeruli, the proximal tubule and the distal tubule. We found extensive decrease and damage in claudin 5, protein located at the glomerular capillaries and in claudin 2, intercellular protein of the proximal tubule. In distal tubules we found increment in claudins 4 and 8, but not delocalization of these proteins. These lesions were observed in the presence of oxidative stress which has been also described in the diabetic patient. The glomerular and the proximal tubular damage were ameliorated by the prevention of oxidative stress.
Indiana University Health, USA
Time : 11:15-12:00
Andrew L Lobashevsky has completed his PhD from Moscow Medical Academy, Russia and Postdoctoral studies from University of Tennessee at Memphis. He is the Associate Professor and Director of histocompatibility and transplant immunology laboratory at Indiana University and IU Health Inc. He has published more than 50 papers in reputed journals and has been serving as an Editorial Board Member of two repute journals.
Donor human leukocyte antigen (HLA)-specific antibodies (DSA) play an important role in solid organ transplantation. Preexisting IgG isotype DSA are considered a risk factor for antibody mediated rejection, graft failure or graft loss. The post-transplant development of DSA depends on multiple factors including immunogenicity of mismatched antigens, HLA class II typing of the recipient, cytokine gene polymorphisms, and cellular immunoregulatory mechanisms. Interaction between complementarity determining regions of the antibody and HLA can be detected by mean fluorescence intensity or lysis of cell membrane through activation of complement. These biological functions of alloantibodies strictly depend on amino acid residue composition of functional and structural epitopes of the antigen. De novo developed antibodies require special attention because not all DSA have equal clinical significance. Therefore, it is important for transplant clinicians and transplant immunologists to accurately characterize DSA. In this talk the contemporary immunological techniques for detection and characterization of anti-HLA antibodies and their pitfalls are presented.