Research topics
The innate immunity system is specialized in the detection of danger signals, either endogenous (dying cells) or exogenous (microbes). Innate immunity, that involves a complex network of cells and soluble molecules, is involved in the initiation of protective responses against microbes and in maintaining or restoring (wound healing) tissue homeostasis. Any alteration of the innate immune system may have severe consequences, such as autoimmunity or chronic inflammation.
Myeloid cells are pivotal in the immune response. Among other mechanisms, they are involved in the elimination of microbes and dying cells as well as in the functional polarization of adaptive cells. Myeloid cells discriminate self from non self (microbes) and modified self (dying cells) using a restricted set of cellular and soluble receptors (pattern recognition molecules or PRM).
Our team is interested in the biology of macrophages and of soluble PRM. Present in all tissues, macrophages are sentinels of the innate immune system. Involved in the regulation of adaptive immune responses, these cells are characterized by a functional plasticity (capacity to adapt their functions to the nature of the local environment). Soluble PRMs act as bridging molecules between macrophages and the elements that have to be phagocytosed.
Our main objectives are:
– To decipher the cellular and molecular mechanisls involved in fucntional polarization of macrophages,
– To identify strategies targeting tumor-associated macrophages,
– To understand the role of some soluble PRM in the detection of danger signals and in the regulation of immune responses.
Each project includes fundamental and translational research.
Staff
Y. Delneste, DR INSERM
P. Jeannin, PU-PH
J. Tabiasco, CR Inserm
D. Couez, PU
A. Morel PU
N. Ifrah, PU-PH
J.F. Subra, PU-PH
P. Guardiola, PU-PH
I. Pellier, PU-PH
A. Schmidt-Tanguy, MCU-PH
A. Chevailler, MCU-PH
C. Beauvillain, MCU-PH
J.F. Augusto, MCU-PH
L. Aymeric, MCU
L. Basset, Post-Doctorant
L. Paolini, Doctorant
V. Larochette, Doctorant
V. Thépot, Doctorant
C. Adam, Doctorant
C.Poli, Doctorant
C. Orvain, Doctorant
A. Bouvier, Doctorant
D. Luque Paz, Doctorant
L. Papargyris, Doctorant
A. Billaud, Doctorant
P. Pignon, AI INSERM
L. Preisser, IR UNIV
S. Blanchard, TN CHU
S. Salle, AI CDD INSERM
Representative publications
– d’Almeida S, Kauffenstein G, Roy C, Basset L, Papargyris L, Henrion D, Catros V, Ifrah N, Descamps P, Croue A, Jeannin P, Gregoire M, Delneste Y, Tabiasco J. Acquisition of immunoregulatory phenotype by tumor-associated macrophages depends on CD39 ecto-ATPDase expression – an IL-27-dependent mechanism. Oncoimmunology (2016)
http://www.hal.inserm.fr/inserm-01385209
– Foucher ED, Blanchard S, Preisser L, Descamps P, Ifrah N, Delneste Y, Jeannin P. IL-34 and M-CSF induce macrophages that switch memory T cells into Th17 cells via membrane IL-1. Eur J Immunol. (2015)
– Miot C, Beaumont E, Duluc D, Le Guillou-Guillemette H, Preisser L, Garo E, Blanchard S, Hubert Fouchard I, Créminon C, Lamourette L, Calès P, Lunel-Fabiani F, Boursier J, Braum O, Fickenscher H, Roingeard P, Delneste Y, Jeannin P. IL-26 is overexpressed in chronically HCV-infected patients and enhances TRAIL-mediated cytotoxicity and interferon production by human NK cells. Gut. (2013)
– Pellier I, Renier G, Rakotonjanahary J, Audrain M, Berardi E, Gardembas M, Clavert A, Moles MP, Proust-Houdemont S, Reguerre Y, De Carli E, Medge M, Garo E, Blanchard S, Miot C, Picard C, Delneste Y, Fischer A, Tanguy-Schmidt A, Jeannin P. Long term consequences of Hodgkin’s lymphoma therapy on T cell lymphopoiesis. J Allergy Clin Immunol. (2015)
– Preisser L, Miot C, Le Guillou H, Beaumont E, Garo E, Blanchard S, Croué A, Fouchard I, Lunel-Fabiani F, Roingeard P, Calès P, Delneste Y, Jeannin P. IL-34 and M-CSF are overexpressed in HCV fibrosis and induce pro-fibrotic macrophages which promote collagen synthesis by hepatic stellate cells. Hepatology. (2014)
– Corvaisier M, Delneste Y, Jeanvoine H, Preisser L, Blanchard S, Garo E, Hoppe E, Barré B, Audran M, Bouvard B, Saint-André JP, Jeannin P. IL-26 is over-expressed in rheumatoid arthritis and induces proinflammatory cytokine production and Th17 cell generation. PLoS Biology. (2012)
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