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Béatrice Pérarnau

Researcher at Pasteur Institute

Publications -  11
Citations -  2030

Béatrice Pérarnau is an academic researcher from Pasteur Institute. The author has contributed to research in topics: CD8 & MHC class I. The author has an hindex of 10, co-authored 11 publications receiving 1992 citations. Previous affiliations of Béatrice Pérarnau include French Institute of Health and Medical Research.

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Journal ArticleDOI

Differential Requirements for Survival and Proliferation of CD8 Naïve or Memory T Cells

TL;DR: Maintenance of CD8 T cell memory still required TCR-MHC class I interactions, but memory T cells may have a lower functional activation threshold that facilitates secondary responses.
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HLA-A2.1–restricted Education and Cytolytic Activity of CD8+ T Lymphocytes from β2 Microglobulin (β2m) HLA-A2.1 Monochain Transgenic H-2Db β2m Double Knockout Mice

TL;DR: Three different HLA-A2.1 monochains were engineered in which either the human or mouse β2-microglobulin (β2m) is covalently linked to the NH2 terminus of the heavy chain by a 15– amino acid long peptide, and the selected HHD construct was introduced by transgenesis in H-2Db/− β2m−/− double knockout mice.
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Single H2Kb, H2Db and double H2KbDb knockout mice: peripheral CD8+ T cell repertoire and anti-lymphocytic choriomeningitis virus cytolytic responses.

TL;DR: Choriomeningitis of H2Db KO mice was linked to the development of a subdominant H2Kb‐restricted cytotoxic T lymphocyte response and should represent useful tools to evaluate the immunological potentials of individual MHC class I molecules.
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Major histocompatibility complex (MHC) class I KbDb −/− deficient mice possess functional CD8+ T cells and natural killer cells

TL;DR: A minor population of functionally competent peripheral CD8+ T cells capable of strong cytotoxic activity arises in the complete absence of classical MHC class Ia molecules.
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MHC class Ia-restricted T cells partially account for beta 2- microglobulin-dependent resistance to Mycobacterium tuberculosis

TL;DR: In this paper, the role of MHC class Ia in resistance to M. tuberculosis infection in mice has been defined, and the authors found that mice deficient in a single MHC-class Ia molecule, either H2-K(b) or H2D(b), were essentially identical to that observed in wild-type mice.