Systemic sclerosis (SSc) involve an aberrant immune response causing chronic inflammation. The INSERM unit U1313 IRATI hypothesizes a global defect in the innate T cells (ITC) in SSc, possibly linked to chronic stimulation by common innate signals. The study aims to compare ITC subsets in SSc patients and healthy volunteers, assess associations with ITC exhaustion/desensitization, and measure connections between ITC abnormalities and SSc-related factors. 

This research contributes to understanding molecular components in the regulation of innate immunity in SSc.

The Monkeypox virus, that causes an emerging zoonosis, initially affects animals such as rodents, has evolved to infect humans. Present mainly in Central and West Africa, the infection is claiming many victims. Generating symptoms similar to human smallpox, with a lower lethality rate, the recent European epidemic of 2022 calls for greater knowledge of the virus infection's physiopathology.

The purpose of the Inflammation, Epithelial Tissues and Cytokines Laboratory of Poitiers is to study Monkeypox viral replication in cutaneous and pulmonary tissues, as well as the cytokine and cellular response set up by the immune system.

Tuberculosis is a pathology caused by Mycobacterium tuberculosis in humans and Mycobacterium bovis in cattle. It is characterized by the presence of granulomas in the lungs, formed by the structured aggregation of immune cells allowing bacteria to be retained. Two populations of neutrophils are involved in these lung lesions: inflammatory and regulatory neutrophils. The objective is to characterize the structure and composition of lung lesions developed by mice during mycobacterial infections and to evaluate the role of regulatory and inflammatory neutrophils in the formation of granulomas.

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The focus is on understanding how the intracellular bacterial pathogen Coxiella burnetii, responsible for Q fever, a zoonosis breathing in dust that has been contaminated by infected animal, manipulates host-pathogen interactions to establish replicative niches. The identified effector protein, EmpA, localized in the nucleus, exhibits structural homology with ATRIP involved in DNA damage repair. 

The aim is to characterize EmpA's mode of action and unravel Coxiella's manipulation of the DNA damage response.

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Schistosomiasis, a neglected tropical disease caused by Schistosoma parasites, relies on Biomphalaria glabrata as an intermediate host for its life cycle. Research highlights the critical role of selective pressures in host-parasite interactions and underlines the molecular mechanisms of compatibility in sympatric and allopatric conditions. This polymorphism observed in natural populations, affecting immune defence in B. glabrata and virulence in S. mansoni. While omics studies have explored this, the role of miRNAs, which are regulators of gene expression, remains overlooked in invertebrate’s immunity. The COMPAMIR project aims to elucidate the miRNome of the immune compartment of B. glabrata, identifying miRNAs as potential biomarkers of compatibility across allopatric gradient in a comparative approach.

This project aims to explore the role of bacteria in health, focusing on the type IV secretion system (T4SS). T4SS are protein complexes found in certain bacteria that enable them to transmit molecules such as proteins, DNA or other components directly to other cells. These systems play an essential role in various biological processes, including the virulence of pathogenic bacteria and bacterial conjugation.

As the precise mechanism governing effector recruitment is still a mystery, the aims of this internship will firstly be to purify the active form of the VirD4 protein, the translocase of the machinery. Secondly, to study the mechanisms of effector recruitment via the IcmSW, LvgA and DotM-dependent pathways in L. pneumophila.