CV Science

Jean-Charles Guéry PhD Immunology, HDR, DR1 INSERM

Course and current status

2021-present:  DR1 INSERM, Group leader "Sex differences in immunity: mechanisms and pathophysiology", INSERM U1291, CNRS U5051, INFINITY, Toulouse

2016-2020:  DR1 INSERM, Group leader "Sex differences in immunity: mechanisms and pathophysiology", INSERM U1043, CNRS U5282, CPTP, Toulouse

2011-2015:   Group leader "Estrogens & calcium channels in autoimmunity and allergy",                         INSERM U1043, CNRS U5282, CPTP, Toulouse

2002-2010: Group leader at INSERM U563 (Dir. G. Delsol), CPTP, Toulouse

1995-2001: Group leader (CR/DR2 INSERM), INSERM U28 (Dir. Ph. Druet), Toulouse

1993-1995: Senior post-doc (Dr L. Adorini), Roche Milano Ricerche, Milano, Italie

1990-1992: Post-doc fellow (Dr L. Adorini), Sandoz Pharma Ltd, CH-4002 Basel, Switzerland

1989-1990: Head Immunotoxicology Unit, Institut de Recherche sur la Sécutité du Médicament, Rhône-Poulenc Santé, Paris.

Scientific summary

From 1991-1995, as a post-doctoral fellow in Dr Luciano Adorini’s lab, I have been studying several aspects of self and non-self antigen presentation by dendritic cells and their impact on tolerance induction and immunity. In this field, I contributed to define the in vivo mechanisms of MHC class II-specific peptide blockers as selective inhibitors of CD4 T cell responses.  I also demonstrated that chronic sustained soluble antigen administration is a selective trigger of Th2 responses in vivo

Since 1996, I established my research group in Toulouse focused on the study of the regulation of T helper cell activation and differentiation, particularly Th2 cells, in experimental models of allotransplantation and allergic diseases. In the context of allotransplantation, we showed that cytotoxic lymphocytes (CTL, NK cells) have important regulatory functions through their capacity to eliminate, whithin draining lymph nodes, donor-derived dendritic cells bearing allo-MHC products. Regarding Th2-cell mediated immune disorders, we identified a sub-class of Ca-channels, specifically expressed by Th2-cells and implicated in their Th2 effector functions. We then demonstrated that they represent potential therapeutic targets for the treatment of allergic diseases.

The current projects of my research group mainly focus on the understanding og the mechanisms responsible for sex-related differences in immunity. The nature and strength of the immune response differ between women and men, resulting in sex-based differences in the prevalence, manifestations and outcome of various autoimmune diseases and allergies. While women are able to mount more vigorous immune responses to infections, they also suffer more from autoimmune and allergic diseases as well as inflammation-induced tissue damages. Our working hypothesis is that sex-linked factors, including sex hormones and sex-chromosome loci, may act in a cell-intrinsic manner to regulate the development, maintenance or functional responses of specific cellular subsets of the innate and adaptive immune system, thereby controlling the sex difference in immune related disorders or susceptibility to infections.  In particular, using genetic models and cell culture systems, we have been studying the role of sex hormone receptors in i) dendritic cell development/function, ii) in the control of Th17-associated central nervous system autoimmunity, and iii) in allergic asthma. Recently, we have shown that androgens inhibit the development of type 2 inflammation in the lungs by negatively regulating the number of ILC2 (group 2 innate lymphoid cells) via the androgen receptor (Laffont et al, J. Exp Med 2017). These findings may explain the sex differences in the prevalence of allergic asthma in Human.