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Article: The Influence of Sex Hormones and X Chromosome in Immune Responses.

Anesi, Nina / Miquel, Charles-Henry / Laffont, Sophie / Guéry, Jean-Charles

Current topics in microbiology and immunology

2023 Volume 441, Page(s) 21–59

Abstract: Males and females differ in their susceptibility to develop autoimmunity and allergy but also in their capacity to cope with infections and cancers. Cellular targets and molecular pathways underlying sexual dimorphism in immunity have started to emerge ... ...

Abstract	Males and females differ in their susceptibility to develop autoimmunity and allergy but also in their capacity to cope with infections and cancers. Cellular targets and molecular pathways underlying sexual dimorphism in immunity have started to emerge and appeared multifactorial. It became increasingly clear that sex-linked biological factors have important impact on the development, tissue maintenance and effector function acquisition of distinct immune cell populations, thereby regulating multiple layers of innate or adaptive immunity through distinct mechanisms. This review discusses the recent development in our understanding of the cell-intrinsic actions of biological factors linked to sex, sex hormones and sex chromosome complement, on immune cells, which may account for the sex differences in susceptibility to autoimmune diseases and allergies, and the sex-biased responses in natural immunity and cancer.
MeSH term(s)	Female ; Male ; Humans ; X Chromosome ; Gonadal Steroid Hormones/genetics ; Autoimmune Diseases/genetics ; Hypersensitivity ; Adaptive Immunity
Chemical Substances	Gonadal Steroid Hormones
Language	English
Publishing date	2023-09-11
Publishing country	Germany
Document type	Review ; Journal Article
ZDB-ID	210099-X
ISSN	0070-217X
ISSN	0070-217X
DOI	10.1007/978-3-031-35139-6_2
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Article ; Online: Deconstructing the sex bias in allergy and autoimmunity: From sex hormones and beyond.

Laffont, Sophie / Guéry, Jean-Charles

Advances in immunology

2019 Volume 142, Page(s) 35–64

Abstract: Men and women differ in their susceptibility to develop autoimmunity and allergy but also in their capacity to cope with infections. Mechanisms responsible for this sexual dimorphism are still poorly documented and probably multifactorial. This review ... ...

Abstract	Men and women differ in their susceptibility to develop autoimmunity and allergy but also in their capacity to cope with infections. Mechanisms responsible for this sexual dimorphism are still poorly documented and probably multifactorial. This review discusses the recent development in our understanding of the cell-intrinsic actions of biological factors linked to sex, sex hormones and sex chromosome complement, on immune cells, which may account for the sex differences in the enhanced susceptibility of women to develop immunological disorders, such as allergic asthma or systemic lupus erythematosus (SLE). We choose to more specifically discuss the impact of sex hormones on the development and function of immune cell populations directly involved in type-2 immunity, and the role of the X-linked Toll like receptor 7 (TLR7) in anti-viral immunity and in SLE. We will also elaborate on the recent evidence demonstrating that TLR7 escapes from X chromosome inactivation in the immune cells of women, and how this may contribute to endow woman immune system with enhanced responsiveness to RNA-virus and susceptibility to SLE.
MeSH term(s)	Animals ; Asthma/etiology ; Asthma/genetics ; Asthma/immunology ; Asthma/metabolism ; Autoimmunity ; Female ; Gonadal Steroid Hormones/genetics ; Gonadal Steroid Hormones/metabolism ; Gonadal Steroid Hormones/physiology ; Humans ; Hypersensitivity/etiology ; Hypersensitivity/genetics ; Immunity, Innate/genetics ; Lupus Erythematosus, Systemic/etiology ; Male ; Microbiota/immunology ; RNA Virus Infections/immunology ; Receptors, Steroid/physiology ; Sex Characteristics ; Toll-Like Receptor 7/physiology ; X Chromosome
Chemical Substances	Gonadal Steroid Hormones ; Receptors, Steroid ; TLR7 protein, human ; Toll-Like Receptor 7
Language	English
Publishing date	2019-05-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80226-8
ISSN	1557-8445 ; 0065-2776
ISSN (online)	1557-8445
ISSN	0065-2776
DOI	10.1016/bs.ai.2019.04.001
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Article ; Online: Sex hormone regulation of innate lymphoid cells

Eve Blanquart / Sophie Laffont / Jean-Charles Guéry

Biomedical Journal, Vol 44, Iss 2, Pp 144-

2021 Volume 156

Abstract: Innate lymphoid cell (ILC) subsets at barrier surfaces contribute to maintain tissue homeostasis and appropriate responses to infection. ILCs respond to environmental factors produced by non-hematopoietic cells within tissues, but also circulating ... ...

Abstract	Innate lymphoid cell (ILC) subsets at barrier surfaces contribute to maintain tissue homeostasis and appropriate responses to infection. ILCs respond to environmental factors produced by non-hematopoietic cells within tissues, but also circulating cytokines or dietary compounds which allow them to adapt to organ milieu. Among these extrinsic signals, evidence is emerging that sex steroid hormones may act in a cell-intrinsic manner to regulate the development, maintenance in tissues and effector functions of specific subsets of ILCs. Understanding the nature and molecular mechanisms of sex steroid hormone actions on ILCs is important to unravel the cause of sexual disparity in human diseases and could lead to new drug development for the treatment of chronic inflammatory diseases or cancers. This review discusses the recent development in our understanding of the cell-intrinsic actions of sex steroid hormones on ILCs and their consequences on tissue-specific immunity with a particular focus on group 2 innate lymphoid cells and NK cells.
Keywords	Sex differences ; Estrogen receptors ; Androgen receptor ; Allergic asthma ; Group 2 innate lymphoid cells ; NK cells ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Sex hormone regulation of innate lymphoid cells.

Blanquart, Eve / Laffont, Sophie / Guéry, Jean-Charles

Biomedical journal

2020 Volume 44, Issue 2, Page(s) 144–156

Abstract	Innate lymphoid cell (ILC) subsets at barrier surfaces contribute to maintain tissue homeostasis and appropriate responses to infection. ILCs respond to environmental factors produced by non-hematopoietic cells within tissues, but also circulating cytokines or dietary compounds which allow them to adapt to organ milieu. Among these extrinsic signals, evidence is emerging that sex steroid hormones may act in a cell-intrinsic manner to regulate the development, maintenance in tissues and effector functions of specific subsets of ILCs. Understanding the nature and molecular mechanisms of sex steroid hormone actions on ILCs is important to unravel the cause of sexual disparity in human diseases and could lead to new drug development for the treatment of chronic inflammatory diseases or cancers. This review discusses the recent development in our understanding of the cell-intrinsic actions of sex steroid hormones on ILCs and their consequences on tissue-specific immunity with a particular focus on group 2 innate lymphoid cells and NK cells.
MeSH term(s)	Cytokines ; Gonadal Steroid Hormones ; Homeostasis ; Humans ; Immunity, Innate ; Lymphocytes
Chemical Substances	Cytokines ; Gonadal Steroid Hormones
Language	English
Publishing date	2020-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2698541-X
ISSN	2320-2890 ; 2320-2890
ISSN (online)	2320-2890
ISSN	2320-2890
DOI	10.1016/j.bj.2020.11.007
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Biais de sexe dans l’asthme allergique - Androgènes et cellules lymphoïdes innées de groupe 2.

Laffont, Sophie / Blanquart, Eve / Guéry, Jean-Charles

Medecine sciences : M/S

2018 Volume 34, Issue 3, Page(s) 247–252

Abstract: Allergic asthma is a chronic pulmonary inflammatory disease initiated by exposure to normally harmless allergens and marked by bronchial hyperreactivity. It affects more than 300 million people worldwide. Asthma often starts in childhood. Epidemiological ...

Title translation	Sex-bias in allergic asthma: androgens and group 2 innate lymphoid cells.
Abstract	Allergic asthma is a chronic pulmonary inflammatory disease initiated by exposure to normally harmless allergens and marked by bronchial hyperreactivity. It affects more than 300 million people worldwide. Asthma often starts in childhood. Epidemiological studies show that there are sexual disparities in the prevalence and severity of asthma. Before the age of 10, the disease is more common in boys. This tendency reverses at puberty suggesting a regulating role of the sex hormones. In this synthesis, we summarize current knowledge on the role of sex hormones in allergic inflammation, with a particular focus on the impact of androgens on the development and function of recently introduced group 2 innate lymphoid cell subsets (ILC2) as critical actors in the initiation of allergic responses.♢.
MeSH term(s)	Androgens/physiology ; Animals ; Asthma/epidemiology ; Asthma/etiology ; Female ; Humans ; Hypersensitivity/complications ; Hypersensitivity/epidemiology ; Hypersensitivity/etiology ; Immunity, Innate/physiology ; Lymphocytes/physiology ; Male ; Prevalence ; Sex Distribution
Chemical Substances	Androgens
Language	French
Publishing date	2018-03-16
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/20183403013
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Article: 188

Garin, Etienne / Palard, Xavier / Rolland, Yan / Le Sourd, Samuel / Lepareur, Nicolas / Ardisson, Valérie / Bouvry, Christelle / Laffont, Sophie / Campillo-Gimenez, Boris / Bellissant, Eric / Edeline, Julien

Cancers

2023 Volume 15, Issue 8

Abstract: Background: Despite the wide development of : Method: Lip-Re-01 was an activity-escalation Phase 1 study involving HCC patients progressing after sorafenib. The primary endpoint was safety based on Common Terminology Criteria for Adverse Events (AEs) ...

Abstract	Background: Despite the wide development of Method: Lip-Re-01 was an activity-escalation Phase 1 study involving HCC patients progressing after sorafenib. The primary endpoint was safety based on Common Terminology Criteria for Adverse Events (AEs) of Grade ≥3 within 2 months. Secondary endpoints included bio-distribution assessed by scintigraphy quantification from 1 to 72 h, tumor to non-tumor uptake ratio (T/NT), as well as blood, urine and feces collection over 72 h, dosimetry, and response evaluation (mRECIST). Results: Overall, 14 heavily pre-treated HCC patients were treated using a whole liver approach. The mean injected activity was 1.5 ± 0.4 GBq for activity Level 1 ( Conclusion: The high in vivo stability of
Language	English
Publishing date	2023-04-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15082245
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Article ; Online: Monocytes are the main source of STING-mediated IFN-α production.

Congy-Jolivet, Nicolas / Cenac, Claire / Dellacasagrande, Jérôme / Puissant-Lubrano, Bénédicte / Apoil, Pol André / Guedj, Kevin / Abbas, Flora / Laffont, Sophie / Sourdet, Sandrine / Guyonnet, Sophie / Nourhashemi, Fati / Guéry, Jean-Charles / Blancher, Antoine

EBioMedicine

2022 Volume 80, Page(s) 104047

Abstract: Background: Type I interferon (IFN-I) production by plasmacytoid dendritic cells (pDCs) occurs during viral infection, in response to Toll-like receptor 7 (TLR7) stimulation and is more vigorous in females than in males. Whether this sex bias persists ... ...

Abstract	Background: Type I interferon (IFN-I) production by plasmacytoid dendritic cells (pDCs) occurs during viral infection, in response to Toll-like receptor 7 (TLR7) stimulation and is more vigorous in females than in males. Whether this sex bias persists in ageing people is currently unknown. In this study, we investigated the effect of sex and aging on IFN-α production induced by PRR agonist ligands. Methods: In a large cohort of individuals from 19 to 97 years old, we measured the production of IFN-α and inflammatory cytokines in whole-blood upon stimulation with either R-848, ODN M362 CpG-C, or cGAMP, which activate the TLR7/8, TLR9 or STING pathways, respectively. We further characterized the cellular sources of IFN-α. Findings: We observed a female predominance in IFN-α production by pDCs in response to TLR7 or TLR9 ligands. The higher TLR7-driven IFN-α production in females was robustly maintained across ages, including the elderly. The sex-bias in TLR9-driven interferon production was lost after age 60, which correlated with the decline in circulating pDCs. By contrast, STING-driven IFN-α production was similar in both sexes, preserved with aging, and correlated with circulating monocyte numbers. Indeed, monocytes were the primary cellular source of IFN-α in response to cGAMP. Interpretation: We show that the sex bias in the TLR7-induced IFN-I production is strongly maintained through ages, and identify monocytes as the main source of IFN-I production via STING pathway. Funding: This work was supported by grants from Région Occitanie/Pyrénées-Méditerranée (#12052910, Inspire Program #1901175), University Paul Sabatier, and the European Regional Development Fund (MP0022856).
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Female ; Humans ; Interferon-alpha/biosynthesis ; Interferon-alpha/blood ; Interferon-alpha/immunology ; Ligands ; Male ; Membrane Proteins/blood ; Membrane Proteins/immunology ; Middle Aged ; Monocytes/immunology ; Monocytes/metabolism ; Toll-Like Receptor 7 ; Toll-Like Receptor 9/metabolism ; Young Adult
Chemical Substances	Interferon-alpha ; Ligands ; Membrane Proteins ; STING1 protein, human ; Toll-Like Receptor 7 ; Toll-Like Receptor 9
Language	English
Publishing date	2022-05-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2022.104047
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Article: Estrogen Receptor-Dependent Regulation of Dendritic Cell Development and Function.

Laffont, Sophie / Seillet, Cyril / Guéry, Jean-Charles

Frontiers in immunology

2017 Volume 8, Page(s) 108

Abstract: Autoimmunity, infectious diseases and cancer affect women and men differently. Because they tend to develop more vigorous adaptive immune responses than men, women are less susceptible to some infectious diseases but also at higher risk of autoimmunity. ... ...

Abstract	Autoimmunity, infectious diseases and cancer affect women and men differently. Because they tend to develop more vigorous adaptive immune responses than men, women are less susceptible to some infectious diseases but also at higher risk of autoimmunity. The regulation of immune responses by sex-dependent factors probably involves several non-redundant mechanisms. A privileged area of study, however, concerns the role of sex steroid hormones in the biology of innate immune cells, especially dendritic cells (DCs). In recent years, our understanding of the lineage origin of DC populations has expanded, and the lineage-committing transcription factors shaping peripheral DC subsets have been identified. Both progenitor cells and mature DC subsets express estrogen receptors (ERs), which are ligand-dependent transcription factors. This suggests that estrogens may contribute to the reported sex differences in immunity by regulating DC biology. Here, we review the recent literature and highlight evidence that estrogen-dependent activation of ERα regulates the development or the functional responses of particular DC subsets. The
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2017.00108
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Article: Sex Differences in Asthma: A Key Role of Androgen-Signaling in Group 2 Innate Lymphoid Cells.

Laffont, Sophie / Blanquart, Eve / Guéry, Jean-Charles

Frontiers in immunology

2017 Volume 8, Page(s) 1069

Abstract: Infectious diseases, autoimmune diseases, and also allergy differentially affect women and men. In general, women develop strongest immune responses and thus the proportion of infected individuals and the severity of many viral, bacterial, or parasitic ... ...

Abstract	Infectious diseases, autoimmune diseases, and also allergy differentially affect women and men. In general, women develop strongest immune responses and thus the proportion of infected individuals and the severity of many viral, bacterial, or parasitic infections are increased in men. However, heightened immunity in women makes them more susceptible than men to autoimmunity and allergy. While sex differences in immunity are well documented, little is known about the cellular and molecular mechanisms underlying these immunological differences, particularly in allergic asthma. Asthma is a chronic inflammation of the airways mediated by exacerbated type 2 immune responses. Sex differences have been reported in the incidence, prevalence, and severity of asthma. While during childhood, males are more susceptible to asthma than females, there is a switch at the onset of puberty as for many other allergic diseases. This decrease of asthma incidence around puberty in males suggests that hormonal mediators could play a protective role in the susceptibility to allergic responses in male. Group 2 innate lymphoid cells (ILC2s) have recently emerged as critical players in the initiation of allergic responses, but also in the resolution of parasitic infection, through their capacity to rapidly and potently produce type 2 cytokines. This review will cover the current understanding of the impact of sex-linked factors in allergic inflammation, with a particular focus on the role of sex hormones on the development and function of tissue-resident ILC2s.
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2017.01069
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Article ; Online: Sexual dimorphism in skin immunity is mediated by an androgen-ILC2-dendritic cell axis.

Science (New York, N.Y.)

2024 Volume 384, Issue 6692, Page(s) eadk6200

Abstract: Males and females exhibit profound differences in immune responses and disease susceptibility. However, the factors responsible for sex differences in tissue immunity remain poorly understood. Here, we uncovered a dominant role for type 2 innate lymphoid ...

Abstract	Males and females exhibit profound differences in immune responses and disease susceptibility. However, the factors responsible for sex differences in tissue immunity remain poorly understood. Here, we uncovered a dominant role for type 2 innate lymphoid cells (ILC2s) in shaping sexual immune dimorphism within the skin. Mechanistically, negative regulation of ILC2s by androgens leads to a reduction in dendritic cell accumulation and activation in males, along with reduced tissue immunity. Collectively, our results reveal a role for the androgen-ILC2-dendritic cell axis in controlling sexual immune dimorphism. Moreover, this work proposes that tissue immune set points are defined by the dual action of sex hormones and the microbiota, with sex hormones controlling the strength of local immunity and microbiota calibrating its tone.
MeSH term(s)	Female ; Male ; Androgens/metabolism ; Dendritic Cells/immunology ; Gonadal Steroid Hormones/metabolism ; Immunity, Innate ; Lymphocytes/immunology ; Sex Characteristics ; Skin/immunology ; Animals ; Mice ; Mice, Inbred C57BL ; Microbiota
Chemical Substances	Androgens ; Gonadal Steroid Hormones
Language	English
Publishing date	2024-04-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.adk6200
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