Hédia Kridane‐Miledi

ORCID: 0000-0002-5067-7197
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About
Contact & Profiles
Research Areas
  • T-cell and B-cell Immunology
  • Immune Cell Function and Interaction
  • Immunotherapy and Immune Responses
  • Iron Metabolism and Disorders
  • Systemic Lupus Erythematosus Research
  • Hemoglobinopathies and Related Disorders
  • Child Nutrition and Water Access
  • Herpesvirus Infections and Treatments
  • Cytomegalovirus and herpesvirus research

Hôpital Saint-Vincent-de-Paul
2013-2014

Institut Cochin
2013-2014

Inserm
2013-2014

Institut Gustave Roussy
2014

Institut Pasteur
2012

We have generated a panel of transgenic mice expressing HLA-A*01:03, -A*24:02, -B*08:01, -B*27:05, -B*35:01, -B*44:02, or -C*07:01 as chimeric monochain molecules (i.e., appropriate HLA α1α2 H chain domains fused with mouse α3 domain and covalently linked to human β2-microglobulin). Whereas surface expression several transgenes was markedly reduced in recipient that coexpressed endogenous H-2 class I molecules, substantial all observed lacking molecules. In these transgenic/H-2 null mice, we...

10.4049/jimmunol.1300483 article EN The Journal of Immunology 2013-06-18

HFE , an MHC class Ib molecule that controls iron metabolism, can be directly targeted by cytotoxic TCR αβ T lymphocytes. Transgenic DBA /2 mice expressing, in a Rag 2 KO context, recognizes mouse (m ) were created to further explore the interface of with immune system. ‐transgenic m Hfe WT deleted ‐reactive cells thymus, but fraction reprogrammed able escape deletion. In contrast, deprived molecules mice) or expressing C 282→ Y mutated – most frequent mutation associated human hereditary...

10.1002/eji.201141664 article EN European Journal of Immunology 2012-04-01
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