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Gilbert C FAURE's insight:

This topic is focusing mainly on fundamental systemic immunology.

 

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Mucosal Immunity:

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Immunology and Biotherapies

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Frontiers | Regulatory Roles of Invariant Natural Killer T Cells in Adipose Tissue Inflammation: Defenders Against Obesity-Induced Metabolic Complications | Immunology

Frontiers | Regulatory Roles of Invariant Natural Killer T Cells in Adipose Tissue Inflammation: Defenders Against Obesity-Induced Metabolic Complications | Immunology | Immunology | Scoop.it
Adipose tissue is a metabolic organ that plays a central role in controlling systemic energy homeostasis. Compelling evidence indicates that immune system is closely linked to healthy physiologic functions and pathologic dysfunction of adipose tissue. In obesity, the accumulation of pro-inflammatory responses in adipose tissue subsequently leads to dysfunction of adipose tissue as well as whole body energy homeostasis. Simultaneously, adipose tissue also activates anti-inflammatory responses in an effort to reduce the unfavorable effects of pro-inflammation. Notably, the interplay between adipocytes and resident invariant natural killer T (iNKT) cells is a major component of defensive mechanisms of adipose tissue. iNKT cells are leukocytes that recognize lipids loaded on CD1d as antigens, whereas most other immune cells are activated by peptide antigens. In adipose tissue, adipocytes directly interact with iNKT cells through presenting lipid antigens and stimulate iNKT cell activation to alleviate pro-inflammation. In this review, we provide an overview of the molecular and cellular determinants of obesity-induced adipose tissue inflammation. Specifically, we focus on the roles of iNKT cell-adipocyte interaction in maintaining adipose tissue homeostasis as well as the consequent modulation in systemic energy metabolism. We also briefly discuss future research directions regarding the interplay between adipocytes and adipose iNKT cells in adipose tissue inflammation.
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Frontiers | Functions of CD1d-Restricted Invariant Natural Killer T Cells in Antimicrobial Immunity and Potential Applications for Infection Control | Immunology

Frontiers | Functions of CD1d-Restricted Invariant Natural Killer T Cells in Antimicrobial Immunity and Potential Applications for Infection Control | Immunology | Immunology | Scoop.it
CD1d-restricted invariant natural killer T (iNKT) cells are innate-type lymphocytes that express a T-cell receptor (TCR) containing an invariant alpha chain encoded by the V alpha 14 gene in mice and V alpha 24 gene in humans. These iNKT cells recognize endogenous, microbial, and synthetic glycolipid antigens presented by the major histocompatibility complex (MHC) class I-like molecule CD1d. Upon TCR stimulation by glycolipid antigens, iNKT cells rapidly produce large amounts of cytokines, including interferon-gamma (IFNgamma) and interleukin-4 (IL-4). Activated iNKT cells contribute to host protection against a broad spectrum of microbial pathogens, and glycolipid-mediated stimulation of iNKT cells ameliorates many microbial infections by augmenting innate and acquired immunity. In some cases, however, antigen-activated iNKT cells exacerbate microbial infections by promoting pathogenic inflammation. Therefore, it is important to identify appropriate microbial targets for the application of iNKT cell activation as a treatment or vaccine adjuvant. Many studies have found that iNKT cell activation induces potent adjuvant activities promoting protective vaccine effects. In this review, we summarize the functions of CD1d-restricted iNKT cells in immune responses against microbial pathogens and describe the potential applications of glycolipid-mediated iNKT cell activation for preventing and controlling microbial infections.
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Foxp3+ T reg cells control psoriasiform inflammation by restraining an IFN-I–driven CD8+ T cell response

Foxp3+ T reg cells control psoriasiform inflammation by restraining an IFN-I–driven CD8+ T cell response | Immunology | Scoop.it
![Figure][1]



Psoriasis is a complex inflammatory skin disease affecting ∼3% of the population worldwide. Although type I interferons (IFN-I) are thought to be involved in its pathogenesis, the details of this relationship remain elusive. Here we show that in a murine model of imiquimod-driven psoriatic skin inflammation, Foxp3+ regulatory T cells (T reg cells) control inflammation severity by restraining IFN-I. Depletion of T reg cells induces IFN-I and IFN-stimulated gene expression, and leads to accumulation of CD8+ T cells in lesional skin. Mononuclear phagocytes (MNPs) were the source of IFN-I, and their depletion reversed the effect of T reg cell depletion. Blockade of IFN-I signaling abolished CD8+ T cell infiltration and excess inflammation in the skin of T reg cell–depleted mice. Depletion of CD8+ T cells attenuated pathology, confirming their role as critical effector cells downstream of IFN-I. Our results describe an unexpected role for T reg cells in restraint of an MNP–IFN-I–driven CD8+ T cell response during psoriasiform skin inflammation. These findings highlight a pathway with potential relevance for the treatment of early-stage disease.

[1]: pending:yes
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Frontiers | Thymic Stromal Lymphopoietin Isoforms, Inflammatory Disorders, and Cancer | Immunology

Frontiers | Thymic Stromal Lymphopoietin Isoforms, Inflammatory Disorders, and Cancer | Immunology | Immunology | Scoop.it
Thymic Stromal Lymphopoietin (TSLP) is a pleiotropic cytokine originally isolated from a murine thymic stromal cell line. TSLP exerts its biological effects by binding to a high affinity heteromeric complex composed of TSLPR chain and IL-7R. TSLP is primarily expressed by activated lung and intestinal epithelial cells, keratinocytes, and fibroblasts. However, dendritic cells, mast cells and presumably other immune cells can also produce TSLP. Different groups of investigators have demonstrated the existence of two variants for TSLP in human tissues: the main isoform expressed in steady state is the short form (sf TSLP), which plays a homeostatic role, whereas the long form (lfTSLP) is upregulated in inflammatory conditions. In addition, there is evidence that in pathological conditions TSLP can be cleaved by several endogenous proteases. Several cellular targets for TSLP have been identified, including immune (dendritic cells, ILC2, T and B cells, NKT and Treg cells, eosinophils, neutrophils, basophils, monocytes, mast cells, and macrophages) and non-immune cells (platelets and sensory neurons). TSLP has been originally implicated in a variety of allergic diseases (e.g., atopic dermatitis, bronchial asthma, eosinophilic esophagitis). Emerging evidence indicates that TSLP is also involved in chronic inflammatory (i.e., COPD, celiac disease) and autoimmune (e.g., psoriasis, rheumatoid arthritis) disorders and several cancers. These emerging observations greatly widen th
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Second signals rescue B cells from activation-induced mitochondrial dysfunction and death

Second signals rescue B cells from activation-induced mitochondrial dysfunction and death | Immunology | Scoop.it
B cells need at least two signals to terminally differentiate into antibody-secreting cells. Pierce and colleagues show that persistent exposure to antigen in the absence of T cell help or ‘pathogen pattern motifs’ leads to B cell death via a calcium-dependent ‘metabolic timer’.
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TCR signal strength controls thymic differentiation of iNKT cell subsets

TCR signal strength controls thymic differentiation of iNKT cell subsets | Immunology | Scoop.it
Invariant natural killer T (iNKT) cells can be subsetted by their cytokine profiles, but how they develop in the thymus is unclear. Here the authors show, by analysing mice carrying mutant Zap70 genes, that T cell receptor signaling strength induces epigenetic changes of genes to modulate iNKT...
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IJMS | Free Full-Text | Immune Checkpoints as the Immune System Regulators and Potential Biomarkers in HIV-1 Infection

IJMS | Free Full-Text | Immune Checkpoints as the Immune System Regulators and Potential Biomarkers in HIV-1 Infection | Immunology | Scoop.it
Immune checkpoints are several co-stimulatory and inhibitory pathways that regulate T cell immune responses. Most of the discoveries about immune checkpoints were made in cancer research where inhibitory immune checkpoints cause immune exhaustion and down-regulate anti-tumor responses.
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White Adipose Tissue Is a Reservoir for Memory T Cells and Promotes Protective Memory Responses to Infection

White Adipose Tissue Is a Reservoir for Memory T Cells and Promotes Protective Memory Responses to Infection | Immunology | Scoop.it
The role of adipose tissue in protective immunity is largely unknown. Han et al. reveal
that white adipose tissue is a reservoir for memory T cells endowed with a distinct
functional and metabolic profile.

Via Krishan Maggon
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Revisiting IL-2: Biology and therapeutic prospects

Revisiting IL-2: Biology and therapeutic prospects | Immunology | Scoop.it
Interleukin-2 (IL-2), the first cytokine that was molecularly cloned, was shown to be a T cell growth factor essential for the proliferation of T cells and the generation of effector and memory cells. On the basis of this activity, the earliest therapeutic application of IL-2 was to boost immune responses in cancer patients. Therefore, it was a surprise that genetic deletion of the cytokine or its receptor led not only to the expected immune deficiency but also to systemic autoimmunity and lymphoproliferation. Subsequent studies established that IL-2 is essential for the maintenance of Foxp3+ regulatory T cells (Treg cells), and in its absence, there is a profound deficiency of Treg cells and resulting autoimmunity. We now know that IL-2 promotes the generation, survival, and functional activity of Treg cells and thus has dual and opposing functions: maintaining Treg cells to control immune responses and stimulating conventional T cells to promote immune responses. It is well documented that certain IL-2 conformations result in selective targeting of Treg cells by increasing reliance on CD25 binding while compromising CD122 binding. Recent therapeutic strategies have emerged to use IL-2, monoclonal antibodies to IL-2, or IL-2 variants to boost Treg cell numbers and function to treat autoimmune diseases while dealing with the continuing challenges to minimize the generation of effector and memory cells, natural killer cells, and other innate lymphoid populations.
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Differential Roles of LTβR in Endothelial Cell Subsets for Lymph Node Organogenesis and Maturation

Differential Roles of LTβR in Endothelial Cell Subsets for Lymph Node Organogenesis and Maturation | Immunology | Scoop.it
Cellular cross-talk mediated by lymphotoxin αβ–lymphotoxin β receptor (LTβR) signaling plays a critical role in lymph node (LN) development. Although the major role of LTβR signaling has long been considered to occur in mesenchymal lymphoid tissue organizer cells, a recent study using a VE-cadherincreLtbrfl/fl mouse model suggested that endothelial LTβR signaling contributes to the formation of LNs. However, the detailed roles of LTβR in different endothelial cells (ECs) in LN development remain unknown. Using various cre transgenic mouse models ( Tekcre , a strain targeting ECs, and Lyve1cre , mainly targeting lymphatic ECs), we observed that specific LTβR ablation in Tekcre+ or Lyve1cre+ cells is not required for LN formation. Moreover, double- cre –mediated LTβR depletion does not interrupt LN formation. Nevertheless, TekcreLtbrfl/fl mice exhibit reduced lymphoid tissue inducer cell accumulation at the LN anlagen and impaired LN maturation. Interestingly, a subset of ECs ( VE-cadherin + Tekcre-low/neg ECs) was found to be enriched in transcripts related to hematopoietic cell recruitment and transendothelial migration, resembling LN high ECs in adult animals. Furthermore, endothelial Tek was observed to negatively regulate hematopoietic cell transmigration. Taken together, our data suggest that although Tekcre+ endothelial LTβR is required for the accumulation of hematopoietic cells and full LN maturation, LTβR in VE-cadherin+Tekcre-low/neg ECs in embryos might represent a critical portal-determining factor for LN formation.
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Understanding Immuno-oncology - The Interplay between the Immune System & Cancer

Understanding Immuno-oncology - The Interplay between the Immune System & Cancer | Immunology | Scoop.it
Explaining immuno-oncology; describing what immuno-oncology is, outlining the tumor antigens and immune cells involved in the tumor microenvironment and the mechanisms of immunosurveillance, immunosuppression and cancer immunotherapy.

Via Krishan Maggon
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Inflammation and immune resolution - Taams - 2018 - Clinical & Experimental Immunology - Wiley Online Library

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The costimulatory molecule CD226 signals through VAV1 to amplify TCR signals and promote IL-17 production by CD4+ T cells

The costimulatory molecule CD226 signals through VAV1 to amplify TCR signals and promote IL-17 production by CD4+ T cells | Immunology | Scoop.it
The guanine nucleotide exchange factor VAV1 is required for T cell receptor (TCR) signaling and activation of T cells. By analyzing the VAV1 interactome, Gaud et al . found that VAV1 also interacted with the costimulatory molecule CD226. Engagement of CD226 activated VAV1, which in turn enhanced the TCR-dependent production of the proinflammatory cytokine IL-17 by human T cells. A variant of CD226 that is associated with autoimmune diseases stimulated more VAV1 activity and IL-17 production than did wild-type CD226, demonstrating that VAV1-mediated cross-talk between the CD226 and TCR signaling pathways affects both normal and pathological T cell activation.
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Formation of the Intrathymic Dendritic Cell Pool Requires CCL21-Mediated Recruitment of CCR7+ Progenitors to the Thymus

Formation of the Intrathymic Dendritic Cell Pool Requires CCL21-Mediated Recruitment of CCR7+ Progenitors to the Thymus | Immunology | Scoop.it
During αβ T cell development in the thymus, migration of newly selected CD4+ and CD8+ thymocytes into medullary areas enables tolerance mechanisms to purge the newly selected αβ TCR repertoire of autoreactive specificities. Thymic dendritic cells (DC) play key roles in this process and consist of three distinct subsets that differ in their developmental origins. Thus, plasmacytoid DC and Sirpα+ conventional DC type 2 are extrathymically derived and enter into the thymus via their respective expression of the chemokine receptors CCR9 and CCR2. In contrast, although Sirpα− conventional DC type 1 (cDC1) are known to arise intrathymically from immature progenitors, the precise nature of such thymus-colonizing progenitors and the mechanisms controlling their thymus entry are unclear. In this article, we report a selective reduction in thymic cDC1 in mice lacking the chemokine receptor CCR7. In addition, we show that the thymus contains a CD11c+MHC class II−Sirpα−Flt3+ cDC progenitor population that expresses CCR7, and that migration of these cells to the thymus is impaired in Ccr7−/− mice. Moreover, thymic cDC1 defects in Ccr7−/− mice are mirrored in plt/plt mice, with further analysis of mice individually lacking the CCR7 ligands CCL21Ser ( Ccl21a−/− ) or CCL19 ( Ccl19−/−) demonstrating an essential role for CCR7-CCL21Ser during intrathymic cDC1 development. Collectively, our data support a mechanism in which CCR7-CCL21Ser interactions guide the migration of cDC progenitors to the thymus for correct formation of the intrathymic cDC1 pool.

This article is featured in In This Issue , p.[323][1]

[1]: /lookup/volpage/201/323
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Improved immunity against reinfections

Improved immunity against reinfections | Immunology | Scoop.it
Researchers have discovered a connection between the body's memory cells and a unique protein in the body called purinergic receptor P2RX7, influencing the body's long-term immune system.
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Peripheral Tissue Chemokines: Homeostatic Control of Immune Surveillance T Cells

Peripheral Tissue Chemokines: Homeostatic Control of Immune Surveillance T Cells | Immunology | Scoop.it
Cellular immunity is governed by a complex network of migratory cues that enable appropriate
immune cell responses in a timely and spatially controlled fashion. This review focuses
on the chemokines and their receptors regulating the steady-state localisation of
immune cells within healthy peripheral tissues. Steady-state immune cell traffic is
not well understood but is thought to involve constitutive (homeostatic) chemokines.
The recent discovery of tissue-resident memory T cells (TRM cells) illustrates our
need for understanding how chemokines control immune cell mobilisation and/or retention.
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Frontiers | Activation and Regulation of B Cell Responses by Invariant Natural Killer T Cells | Immunology

Frontiers | Activation and Regulation of B Cell Responses by Invariant Natural Killer T Cells | Immunology | Immunology | Scoop.it
CD1d-restricted invariant natural killer T (iNKT) cells play central roles in the activation and regulation of innate and adaptive immunity. Cytokine-mediated and CD1d-dependent interactions between iNKT cells and myeloid and lymphoid cells enable iNKT cells to contribute to the activation of multiple cell types, with important impacts on host immunity to infection and tumors and on the prevention of autoimmunity. Here we review the mechanisms by which iNKT cells contribute to B cell maturation, antibody and cytokine production, and antigen presentation. Cognate interactions with B cells contribute to the rapid production of antibodies directed against conserved non-protein antigens resulting in rapid but short-lived innate humoral immunity. iNKT cells can also provide non-cognate help for the generation of antibodies directed against protein antigens, by promoting the activation of follicular helper T cells, resulting in long-lasting adaptive humoral immunity and B cell memory. iNKT cells can also regulate humoral immunity by promoting the development of autoreactive B cells into regulatory B cells. Depletions and functional impairments of iNKT cells are found in patients with infectious, autoimmune and malignant diseases associated with altered B cell function and in murine models of these conditions. The adjuvant and regulatory activities that iNKT cells have for B cells makes them attractive therapeutic targets for these diseases.
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Shedding of CD16 disassembles the NK cell immune synapse and boosts serial engagement of target cells

Shedding of CD16 disassembles the NK cell immune synapse and boosts serial engagement of target cells | Immunology | Scoop.it
Natural Killer (NK) cells can engage multiple virally infected or tumor cells sequentially and deliver perforin for cytolytic killing of these targets. Using microscopy to visualize degranulation from individual NK cells, we found that repeated activation via the Fc receptor CD16 decreased the amount of perforin secreted. However, perforin secretion was restored upon subsequent activation via a different activating receptor, NKG2D. Repeated stimulation via NKG2D also decreased perforin secretion, but this was not rescued by stimulation via CD16. These different outcomes of sequential stimulation could be accounted for by shedding of CD16 being triggered by cellular activation. The use of pharmacological inhibitors and NK cells transfected to express a noncleavable form of CD16 revealed that CD16 shedding also increased NK cell motility and facilitated detachment of NK cells from target cells. Disassembly of the immune synapse caused by CD16 shedding aided NK cell survival and boosted serial engagement of target cells. Thus, counterintuitively, shedding of CD16 may positively impact immune responses.
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IJMS | Free Full-Text | Molecular Regulation of Differentiation in Early B-Lymphocyte Development

IJMS | Free Full-Text | Molecular Regulation of Differentiation in Early B-Lymphocyte Development | Immunology | Scoop.it
B-lymphocyte differentiation is one of the best understood developmental pathways in the hematopoietic system. Our understanding of the developmental trajectories linking the multipotent hematopoietic stem cell to the mature functional B-lymphocyte is extensive as a result of efforts to identify...
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Type 2 immunity: Expanding our view. - PubMed - NCBI

Type 2 immunity: Expanding our view. - PubMed - NCBI | Immunology | Scoop.it
Sci Immunol. 2018 Jul 6;3(25). pii: eaat1604. doi: 10.1126/sciimmunol.aat1604. Review
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Metabolic signaling directs the reciprocal lineage decisions of αβ and γδ T cells

Metabolic signaling directs the reciprocal lineage decisions of αβ and γδ T cells | Immunology | Scoop.it
Cell differentiation is often accompanied by metabolic changes. Yang et al . report that generation of double-positive (DP) thymocytes from double-negative (DN) cells coincides with dynamic regulation of glycolytic and oxidative metabolism. Given the central role of mechanistic target of rapamycin complex 1 (mTORC1) signaling in regulating metabolic changes, they examined the role of mTORC1 pathway in thymocyte development by conditionally deleting RAPTOR, the key component of the mTORC1 complex, in thymocytes. Loss of RAPTOR impaired the DN-to-DP transition, but unexpectedly also perturbed the balance between αβ and γδ T cells and promoted the generation of γδ T cells. Their studies highlight an unappreciated role for mTORC1-dependent metabolic changes in controlling thymocyte fates.

Via Krishan Maggon
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IL-22: There Is a Gap in Our Knowledge

IL-22: There Is a Gap in Our Knowledge | Immunology | Scoop.it
IL-22 is a critical cytokine in modulating tissue responses during inflammation. IL-22 is upregulated in many chronic inflammatory diseases, making IL-22 biology a potentially rewarding therapeutic target. However, this is complicated by the dual-natured role of IL-22 in inflammation, as the cytokine can be protective or inflammatory depending on the disease model. Although scientific interest in IL-22 has increased considerably in the past 10 y, there is still much we do not know about the environmental, cellular, and molecular factors that regulate the production and function of this cytokine. A better understanding of IL-22 biology will allow us to develop new or improved therapeutics for treating chronic inflammatory diseases. In this article, I will highlight some of the outstanding questions in IL-22 biology.
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Trim33 mediates the proinflammatory function of Th17 cells

Trim33 mediates the proinflammatory function of Th17 cells | Immunology | Scoop.it
Transforming growth factor–β (TGF-β) regulates reciprocal regulatory T cell (T reg) and T helper 17 (Th17) differentiation, the underlying mechanism of which is still not understood. Here, we report that tripartite motif-containing 33 (Trim33), a modulator of TGF-β signaling that associates with Smad2, regulates the proinflammatory function of Th17 cells. Trim33 deficiency in T cells ameliorated an autoimmune disease in vivo . Trim33 was required for induction in vitro of Th17, but not T reg cells. Moreover, Smad4 and Trim33 play contrasting roles in the regulation of IL-10 expression; loss of Trim33 enhanced IL-10 production. Furthermore, Trim33 was recruited to the Il17a and Il10 gene loci, dependent on Smad2, and mediated their chromatin remodeling during Th17 differentiation. Trim33 thus promotes the proinflammatory function of Th17 cells by inducing IL-17 and suppressing IL-10 expression.
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Successful Applicants | British Society for Immunology

Information and announcements on applicatns who have been funded in the Communicating Immunology grants.
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