F
Federico Garrido
Researcher at University of Granada
Publications - 243
Citations - 13174
Federico Garrido is an academic researcher from University of Granada. The author has contributed to research in topics: Human leukocyte antigen & Antigen. The author has an hindex of 58, co-authored 240 publications receiving 12077 citations. Previous affiliations of Federico Garrido include University of Jaén.
Papers
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Journal ArticleDOI
Implications for immunosurveillance of altered hla class i phenotypes in human tumours
Federico Garrido,Francisco Ruiz-Cabello,Teresa Cabrera,Juan J. Pérez-Villar,Miguel López-Botet,Maggie Duggan-Keen,Peter L. Stern +6 more
TL;DR: Altered HLA class I tumour phenotypes are analyzed in detail, indicating their potential relevance for implementation of immunotherapeutic protocols and strategies to overcome tumour escape mechanisms.
Journal ArticleDOI
Natural history of HLA expression during tumour development
Federico Garrido,Teresa Cabrera,Ángel Concha,Susan S. Glew,Francisco Ruiz-Cabello,Peter L. Stern +5 more
TL;DR: Data is presented from a variety of tumour types, suggesting that HLA class I alterations may occur at a particular step between the development of an in situ lesion and an invasive carcinoma.
Journal ArticleDOI
MHC class I antigens, immune surveillance, and tumor immune escape.
TL;DR: The mechanisms that allow CTLs to recognize tumor antigens after antigen processing by transformed cells are updated and data is presented indicating the MHC class I phenotype and the immunogenicity of experimental metastatic tumors change drastically when tumors develop in immunodeficient mice.
Journal ArticleDOI
The urgent need to recover MHC class I in cancers for effective immunotherapy
TL;DR: Three tumor phenotypes determine cancer fate: escape, rejection and dormancy, and recovery of MHC class I expression is required to improve cancer immunotherapy.
Book ChapterDOI
MHC antigens and tumor escape from immune surveillance.
Federico Garrido,Ignacio Algarra +1 more
TL;DR: Experimental data are presented supporting the hypothesis that the MHC class I-negative tumor variants are selected in vivo by cytotoxic lymphocyte (CTL) responses against MHCclass I-positive tumor cells.