@article{36165182,

title = {IgG Subclass-Dependent Pulmonary Antigen Retention during Acute IgG-Dependent Systemic Anaphylaxis in Mice.},

author = {Todorova B and Godon O and Conde E and Gillis CM and Iannascoli B and Richard-Le Goff O and Fiole D and Roumenina LT and Leusen JHW and Murphy AJ and Macdonald LE and Reber LL and Jönsson F and Bruhns P},

url = {https://pubmed.ncbi.nlm.nih.gov/36165182/},

doi = {10.4049/jimmunol.2200234},

year  = {2022},

date = {2022-10-01},

journal = {J Immunol},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{vanJoost.2022,

title = {IL-2 and IL-15 drive intrathymic development of distinct periphery-seeding CD4+Foxp3+ regulatory T lymphocytes},

author = {Cécile Apert and Ariel Galindo-Albarrán and Sarah Castan and Claire Detraves and Héloise Michaud and Nicola McJannett and Bart Haegeman and Simon Fillatreau and Bernard Malissen and Georg Hollander and Saulius Zuklys and Jérémy Santamaria and Olivier Joffre and Paola Romagnoli and Joost van Meerwijk},

url = {https://www.frontiersin.org/articles/10.3389/fimmu.2022.965303/full},

doi = {10.3389/fimmu.2022.965303},

year  = {2022},

date = {2022-09-08},

journal = {Frontiers in Immunology},

abstract = {Development of Foxp3-expressing regulatory T-lymphocytes (Treg) in the thymus is controlled by signals delivered in T-cell precursors via the TCR, co-stimulatory receptors, and cytokine receptors. In absence of IL-2, IL-15 or their receptors, fewer Treg apparently develop in the thymus. However, it was recently shown that a substantial part of thymic Treg are cells that had recirculated from the periphery back to the thymus, troubling interpretation of these results. We therefore reassessed the involvement of IL-2 and IL-15 in the development of Treg, taking into account Treg-recirculation. At the age of three weeks, when in wt and IL-15-deficient (but not in IL-2-deficient) mice substantial amounts of recirculating Treg are present in the thymus, we found similarly reduced proportions of newly developed Treg in absence of IL-2 or IL-15, and in absence of both cytokines even less Treg developed. In neonates, when practically no recirculating Treg were found in the thymus, the absence of IL-2 led to substantially more reduced Treg-development than deficiency in IL-15. IL-2 but not IL-15 modulated the CD25, GITR, OX40, and CD73-phenotypes of the thymus-egress-competent and periphery-seeding Treg-population. Interestingly, IL-2 and IL-15 also modulated the TCR-repertoire expressed by developing Treg. Upon transfer into Treg-less Foxp3sf mice, newly developed Treg from IL-2- (and to a much lesser extent IL-15-) deficient mice suppressed immunopathology less efficiently than wt Treg. Taken together, our results firmly establish important non-redundant quantitative and qualitative roles for IL-2 and, to a lesser extent, IL-15 in intrathymic Treg-development.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Bergamelli2022,

title = {Human Cytomegalovirus Modifies Placental Small Extracellular Vesicle Composition to Enhance Infection of Fetal Neural Cells In Vitro},

author = {Mathilde Bergamelli and Hélène Martin and Yann Aubert and Jean-Michel Mansuy and Marlène Marcellin and Odile Burlet-Schiltz and Ilse Hurbain and Graça Raposo and Jacques Izopet and Thierry Fournier and Alexandra Benchoua and Mélinda Bénard and Marion Groussolles and Géraldine Cartron and Yann Tanguy Le Gac and Nathalie Moinard and Gisela D’Angelo and Cécile E. Malnou},

doi = {10.3390/v14092030},

issn = {1999-4915},

year  = {2022},

date = {2022-09-00},

urldate = {2022-09-00},

journal = {Viruses},

volume = {14},

number = {9},

publisher = {MDPI AG},

abstract = {<jats:p>Although placental small extracellular vesicles (sEVs) are extensively studied in the context of pregnancy, little is known about their role during viral congenital infection, especially at the beginning of pregnancy. In this study, we examined the consequences of human cytomegalovirus (hCMV) infection on sEVs production, composition, and function using an immortalized human cytotrophoblast cell line derived from first trimester placenta. By combining complementary approaches of biochemistry, electron microscopy, and quantitative proteomic analysis, we showed that hCMV infection increases the yield of sEVs produced by cytotrophoblasts and modifies their protein content towards a potential proviral phenotype. We further demonstrate that sEVs secreted by hCMV-infected cytotrophoblasts potentiate infection in naive recipient cells of fetal origin, including human neural stem cells. Importantly, these functional consequences are also observed with sEVs prepared from an ex vivo model of infected histocultures from early placenta. Based on these findings, we propose that placental sEVs could be important actors favoring viral dissemination to the fetal brain during hCMV congenital infection.</jats:p>},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35644112,

title = {Tissue-resident CD8 T cells in central nervous system inflammatory diseases: present at the crime scene and …guilty},

author = {Doron Merkler and Ilena Vincenti and Frederick Masson and Roland S Liblau},

doi = {10.1016/j.coi.2022.102211},

issn = {1879-0372},

year  = {2022},

date = {2022-08-01},

urldate = {2022-08-01},

journal = {Curr Opin Immunol},

volume = {77},

pages = {102211},

abstract = {Tissue-resident memory T cells (T) represent a subset of antigen-experienced T cells that are constantly retained in a given tissue with limited trafficking through the circulation. These cells are characterized by expression of molecules enabling their tissue anchoring and downregulation of molecules promoting tissue egress. They reside at sites of previous antigen encounter and their number increases with age. T have been shown to provide rapid and efficient protection against tissue reinfection and T density correlates with efficient antitumor responses. Intriguingly, the density of CD8 T is increased in the central nervous system (CNS) of patients with neuroinflammatory diseases such as multiple sclerosis, or suffering from neurodegenerative diseases. In this review, we discuss current knowledge regarding the diversity of CNS-resident CD8 T cells and their role in CNS autoimmunity. Given their likely contribution to the protracted course of several inflammatory diseases of the CNS, their therapeutic targeting becomes an important challenge.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Martin2022b,

title = {Usutu Virus Infects Human Placental Explants and Induces Congenital Defects in Mice},

author = {Hélène Martin and Jonathan Barthelemy and Yamileth Chin and Mathilde Bergamelli and Nathalie Moinard and Géraldine Cartron and Yann Tanguy Le Gac and Cécile E. Malnou and Yannick Simonin},

doi = {10.3390/v14081619},

issn = {1999-4915},

year  = {2022},

date = {2022-08-00},

urldate = {2022-08-00},

journal = {Viruses},

volume = {14},

number = {8},

publisher = {MDPI AG},

abstract = {<jats:p>Usutu virus (USUV) is a neurotropic mosquito-borne flavivirus that has dispersed quickly in Europe these past years. This arbovirus mainly follows an enzootic cycle involving mosquitoes and birds, but can also infect other mammals, causing notably sporadic cases in humans. Although it is mainly asymptomatic or responsible for mild clinical symptoms, USUV has been associated with neurological disorders, such as encephalitis and meningoencephalitis, highlighting the potential health threat of this virus. Among the different transmission routes described for other flaviviruses, the capacity for some of them to be transmitted vertically has been demonstrated, notably for Zika virus or West Nile virus, which are closely related to USUV. To evaluate the ability of USUV to replicate in the placenta and gain access to the fetus, we combined the use of several trophoblast model cell lines, ex vivo human placental explant cultures from first and third trimester of pregnancy, and in vivo USUV-infected pregnant mice. Our data demonstrate that human placental cells and tissues are permissive to USUV replication, and suggest that viral transmission can occur in mice during gestation. Hence, our observations suggest that USUV could be efficiently transmitted by the vertical route.</jats:p>},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{2022,

title = {Quelle est la réalité des infections humaines par les Bornavirus ?},

doi = {10.1684/vir.2022.0965},

issn = {1267-8694},

year  = {2022},

date = {2022-07-01},

urldate = {2022-07-01},

journal = {Virologie},

volume = {26},

number = {4},

pages = {275--281},

publisher = {John Libbey Eurotext},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35552381b,

title = {Influenza vaccination induces autoimmunity against orexinergic neurons in a mouse model for narcolepsy},

author = {Raphaël Bernard-Valnet and David Frieser and Xuan Hung Nguyen and Leila Khajavi and Clémence Quériault and Sébastien Arthaud and Silvia Melzi and Maxime Fusade-Boyer and Frederick Masson and Matthias Zytnicki and Abdelhadi Saoudi and Yves Dauvilliers and Christelle Peyron and Jan Bauer and Roland S Liblau},

doi = {10.1093/brain/awab455},

issn = {1460-2156},

year  = {2022},

date = {2022-06-01},

urldate = {2022-06-01},

journal = {Brain},

volume = {145},

number = {6},

pages = {2018--2030},

abstract = {Narcolepsy with cataplexy or narcolepsy type 1 is a disabling chronic sleep disorder resulting from the destruction of orexinergic neurons in the hypothalamus. The tight association of narcolepsy with HLA-DQB1*06:02 strongly suggest an autoimmune origin to this disease. Furthermore, converging epidemiological studies have identified an increased incidence for narcolepsy in Europe following Pandemrix® vaccination against the 2009-2010 pandemic 'influenza' virus strain. The potential immunological link between the Pandemrix® vaccination and narcolepsy remains, however, unknown. Deciphering these mechanisms may reveal pathways potentially at play in most cases of narcolepsy. Here, we developed a mouse model allowing to track and study the T-cell response against 'influenza' virus haemagglutinin, which was selectively expressed in the orexinergic neurons as a new self-antigen. Pandemrix® vaccination in this mouse model resulted in hypothalamic inflammation and selective destruction of orexin-producing neurons. Further investigations on the relative contribution of T-cell subsets in this process revealed that haemagglutinin-specific CD4 T cells were necessary for the development of hypothalamic inflammation, but insufficient for killing orexinergic neurons. Conversely, haemagglutinin-specific CD8 T cells could not initiate inflammation but were the effectors of the destruction of orexinergic neurons. Additional studies revealed pathways potentially involved in the disease process. Notably, the interferon-γ pathway was proven essential, as interferon-γ-deficient CD8 T cells were unable to elicit the loss of orexinergic neurons. Our work demonstrates that an immunopathological process mimicking narcolepsy can be elicited by immune cross-reactivity between a vaccine antigen and a neuronal self-antigen. This process relies on a synergy between autoreactive CD4 and CD8 T cells for disease development. This work furthers our understanding of the mechanisms and pathways potentially involved in the development of a neurological side effect due to a vaccine and, likely, to narcolepsy in general.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35552381,

title = {Influenza vaccination induces autoimmunity against orexinergic neurons in a mouse model for narcolepsy},

author = {Raphaël Bernard-Valnet and David Frieser and Xuan Hung Nguyen and Leila Khajavi and Clémence Quériault and Sébastien Arthaud and Silvia Melzi and Maxime Fusade-Boyer and Frederick Masson and Matthias Zytnicki and Abdelhadi Saoudi and Yves Dauvilliers and Christelle Peyron and Jan Bauer and Roland S Liblau},

doi = {10.1093/brain/awab455},

issn = {1460-2156},

year  = {2022},

date = {2022-06-01},

urldate = {2022-06-01},

journal = {Brain},

volume = {145},

number = {6},

pages = {2018--2030},

abstract = {Narcolepsy with cataplexy or narcolepsy type 1 is a disabling chronic sleep disorder resulting from the destruction of orexinergic neurons in the hypothalamus. The tight association of narcolepsy with HLA-DQB1*06:02 strongly suggest an autoimmune origin to this disease. Furthermore, converging epidemiological studies have identified an increased incidence for narcolepsy in Europe following Pandemrix® vaccination against the 2009-2010 pandemic 'influenza' virus strain. The potential immunological link between the Pandemrix® vaccination and narcolepsy remains, however, unknown. Deciphering these mechanisms may reveal pathways potentially at play in most cases of narcolepsy. Here, we developed a mouse model allowing to track and study the T-cell response against 'influenza' virus haemagglutinin, which was selectively expressed in the orexinergic neurons as a new self-antigen. Pandemrix® vaccination in this mouse model resulted in hypothalamic inflammation and selective destruction of orexin-producing neurons. Further investigations on the relative contribution of T-cell subsets in this process revealed that haemagglutinin-specific CD4 T cells were necessary for the development of hypothalamic inflammation, but insufficient for killing orexinergic neurons. Conversely, haemagglutinin-specific CD8 T cells could not initiate inflammation but were the effectors of the destruction of orexinergic neurons. Additional studies revealed pathways potentially involved in the disease process. Notably, the interferon-γ pathway was proven essential, as interferon-γ-deficient CD8 T cells were unable to elicit the loss of orexinergic neurons. Our work demonstrates that an immunopathological process mimicking narcolepsy can be elicited by immune cross-reactivity between a vaccine antigen and a neuronal self-antigen. This process relies on a synergy between autoreactive CD4 and CD8 T cells for disease development. This work furthers our understanding of the mechanisms and pathways potentially involved in the development of a neurological side effect due to a vaccine and, likely, to narcolepsy in general.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{WPM2022,

title = {The anti-FcεRI antibody MAR-1 depletes basophils and cross-reacts with myeloid cells through its Fc portion},

author = {Worrall WPM, Kamphuis JBJ, Stackowicz J, Mougel A, Mauré E, Pecalvel C, Brûlé S, Bruhns P, Guilleminault L, Reber LL.},

url = {https://pubmed.ncbi.nlm.nih.gov/35244223/},

doi = { 10.1111/all.15269},

year  = {2022},

date = {2022-06-01},

journal = {Allergy},

volume = {77},

number = {6},

pages = {1903-1906},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Gaudenzio2022,

title = {Mast cell-neuron axis in allergy},

author = {Nicolas Gaudenzio, Lilian Basso},

year  = {2022},

date = {2022-05-20},

journal = {Curr Opin Immunol .},

volume = {77},

number = {102213},

pages = {1-6},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{N2022,

title = {Immune cells impede repair of old neurons},

author = {Gaudenzio N, Liblau RS.},

editor = {{Lambert de Rouvroit}, Catherine},

year  = {2022},

date = {2022-05-13},

journal = {Science},

volume = {376},

number = {6594},

pages = { 694-695},

abstract = {The regenerative capacity of older people is reduced, resulting in decreased tissue function and resilience. Accordingly, the regeneration of the sciatic nerve after injury has been reported to be less efficient and slower in older people (1). One of the hallmarks of aging is altered intercellular communication, which is often accompanied by increased density of immune cells within tissues and excessive release of proinflammatory mediators, called inflammaging (2, 3). In this context, the immune system disturbs tissue homeostasis and impedes functional recovery. However, the precise mechanisms underlying this pathophysiological process are largely elusive, which is a barrier to rational treatment design. On page 715 of this issue, Zhou et al. (4) describe a mechanism by which aged sensory neurons release the chemoattractive protein C-X-C motif chemokine ligand 13 (CXCL13). Upon sciatic nerve injury in aged, but not young, mice, this results in the recruitment of CD8+ T cells that prevent axonal regeneration.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35549427,

title = {Immune cells impede repair of old neurons},

author = {Nicolas Gaudenzio and Roland S Liblau},

doi = {10.1126/science.abp9878},

issn = {1095-9203},

year  = {2022},

date = {2022-05-01},

urldate = {2022-05-01},

journal = {Science},

volume = {376},

number = {6594},

pages = {694--695},

abstract = {Interfering with age-related neuroimmune interactions promotes nerve regeneration.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{35394686,

title = {Increased fermentable carbohydrate intake alters colonic mucus barrier function through glycation processes and increased mast cell counts.},

author = {Kamphuis JBJ and Reber LL and Eutamène H and Theodorou V},

url = {https://pubmed.ncbi.nlm.nih.gov/35394686/},

doi = {10.1096/fj.202100494RRR},

year  = {2022},

date = {2022-05-01},

journal = {FASEB J},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35476442,

title = {Toward identification of personalized immunological profiles in multiple sclerosis},

author = {Reinhard Hohlfeld and Roland S Liblau},

doi = {10.1126/sciadv.abq4849},

issn = {2375-2548},

year  = {2022},

date = {2022-04-01},

urldate = {2022-04-01},

journal = {Sci Adv},

volume = {8},

number = {17},

pages = {eabq4849},

abstract = {The diversity of four previously unidentified autoantigens found in multiple sclerosis mirrors its notorious clinical variability.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35417189,

title = {Tissue-resident CD8 T cells drive compartmentalized and chronic autoimmune damage against CNS neurons},

author = {David Frieser and Aurora Pignata and Leila Khajavi and Danielle Shlesinger and Carmen Gonzalez-Fierro and Xuan-Hung Nguyen and Alexander Yermanos and Doron Merkler and Romana Höftberger and Virginie Desestret and Katharina M Mair and Jan Bauer and Frederick Masson and Roland S Liblau},

doi = {10.1126/scitranslmed.abl6157},

issn = {1946-6242},

year  = {2022},

date = {2022-04-01},

urldate = {2022-04-01},

journal = {Sci Transl Med},

volume = {14},

number = {640},

pages = {eabl6157},

abstract = {The mechanisms underlying the chronicity of autoimmune diseases of the central nervous system (CNS) are largely unknown. In particular, it is unclear whether tissue-resident memory T cells (T) contribute to lesion pathogenesis during chronic CNS autoimmunity. Here, we observed that a high frequency of brain-infiltrating CD8 T cells exhibit a T-like phenotype in human autoimmune encephalitis. Using mouse models of neuronal autoimmunity and a combination of T single-cell transcriptomics, high-dimensional flow cytometry, and histopathology, we found that pathogenic CD8 T cells behind the blood-brain barrier adopt a characteristic T differentiation program, and we revealed their phenotypic and functional heterogeneity. In the diseased CNS, autoreactive tissue-resident CD8 T cells sustained focal neuroinflammation and progressive loss of neurons, independently of recirculating CD8 T cells. Consistently, a large fraction of autoreactive tissue-resident CD8 T cells exhibited proliferative potential as well as proinflammatory and cytotoxic properties. Persistence of tissue-resident CD8 T cells in the CNS and their functional output, but not their initial differentiation, were crucially dependent on CD4 T cells. Collectively, our results point to tissue-resident CD8 T cells as essential drivers of chronic CNS autoimmunity and suggest that therapies targeting this compartmentalized autoreactive T cell subset might be effective for treating CNS autoimmune diseases.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{35283171,

title = {Pharmacological approaches to target type 2 cytokines in asthma.},

author = {Guilleminault L and Conde E and Reber LL.},

url = {https://pubmed.ncbi.nlm.nih.gov/35283171/},

doi = {10.1016/j.pharmthera.2022.108167 },

year  = {2022},

date = {2022-03-10},

journal = {Pharmacol Ther},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nicoli_altered_2022b,

title = {Altered Basal Lipid Metabolism Underlies the Functional Impairment of Naive CD8+ Ŧ Cells in Elderly Humans},

author = {Nicoli, Francesco and Cabral-Piccin, Mariela P. and Papagno, Laura and Gallerani, Eleonora and Fusaro, Mathieu and Folcher, Victor and Dubois, Marion and Clave, Emmanuel and Vallet, Hélène and Frere, Justin J. and Gostick, Emma and Llewellyn-Lacey, Sian and Price, David A. and Toubert, Antoine and Dupré, Loïc and Boddaert, Jacques and Caputo, Antonella and Gavioli, Riccardo and Appay, Victor},

doi = {10.4049/jimmunol.2100194},

issn = {1550-6606},

year  = {2022},

date = {2022-02-01},

journal = {J Immunol},

volume = {208},

number = {3},

pages = {562--570},

abstract = {Aging is associated with functional deficits in the naive T cell compartment, which compromise the generation of de novo immune responses against previously unencountered Ags. The mechanisms that underlie this phenomenon have nonetheless remained unclear. We found that naive CD8+ T cells in elderly humans were prone to apoptosis and proliferated suboptimally in response to stimulation via the TCR. These abnormalities were associated with dysregulated lipid metabolism under homeostatic conditions and enhanced levels of basal activation. Importantly, reversal of the bioenergetic anomalies with lipid-altering drugs, such as rosiglitazone, almost completely restored the Ag responsiveness of naive CD8+ T cells. Interventions that favor lipid catabolism may therefore find utility as adjunctive therapies in the elderly to promote vaccine-induced immunity against targetable cancers and emerging pathogens, such as seasonal influenza viruses and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2126,

title = {Repolarization of Unbalanced Macrophages: Unmet Medical Need in Chronic Inflammation and Cancer},

author = {Y. Degboe and R. Poupot and M. Poupot},

url = {https://www.ncbi.nlm.nih.gov/pubmed/35163420},

doi = {10.3390/ijms23031496},

issn = {1422-0067 (Electronic) 1422-0067 (Linking)},

year  = {2022},

date = {2022-01-01},

urldate = {2022-01-01},

journal = {Int J Mol Sci},

volume = {23},

number = {3},

abstract = {Monocytes and their tissue counterpart macrophages (MP) constitute the front line of the immune system. Indeed, they are able to rapidly and efficiently detect both external and internal danger signals, thereby activating the immune system to eradicate the disturbing biological, chemical, or physical agents. They are also in charge of the control of the immune response and account for the repair of the damaged tissues, eventually restoring tissue homeostasis. The balance between these dual activities must be thoroughly controlled in space and time. Any sustained unbalanced response of MP leads to pathological disorders, such as chronic inflammation, or favors cancer development and progression. In this review, we take advantage of our expertise in chronic inflammation, especially in rheumatoid arthritis, and in cancer, to highlight the pivotal role of MP in the physiopathology of these disorders and to emphasize the repolarization of unbalanced MP as a promising therapeutic strategy to control these diseases.},

note = {Degboe, Yannick 

Poupot, Remy 

Poupot, Mary 

eng 

Review 

Switzerland 

2022/02/16 

Int J Mol Sci. 2022 Jan 28;23(3):1496. doi: 10.3390/ijms23031496.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}