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We began analyzing https://link.springer.com/article/10.1007/s00281-021-00842-3, but it redirected us to https://link.springer.com/article/10.1007/s00281-021-00842-3. The analysis below is for the second page.

Title[redir]:
Thymus and autoimmunity | Seminars in Immunopathology
Description:
The thymus prevents autoimmune diseases through mechanisms that operate in the cortex and medulla, comprising positive and negative selection and the generation of regulatory T-cells (Tregs). Egress from the thymus through the perivascular space (PVS) to the blood is another possible checkpoint, as shown by some autoimmune/immunodeficiency syndromes. In polygenic autoimmune diseases, subtle thymic dysfunctions may compound genetic, hormonal and environmental cues. Here, we cover (a) tolerance-inducing cell types, whether thymic epithelial or tuft cells, or dendritic, B- or thymic myoid cells; (b) tolerance-inducing mechanisms and their failure in relation to thymic anatomic compartments, and with special emphasis on human monogenic and polygenic autoimmune diseases and the related thymic pathologies, if known; (c) polymorphisms and mutations of tolerance-related genes with an impact on positive selection (e.g. the gene encoding the thymoproteasome-specific subunit, PSMB11), promiscuous gene expression (e.g. AIRE, PRKDC, FEZF2, CHD4), Treg development (e.g. SATB1, FOXP3), T-cell migration (e.g. TAGAP) and egress from the thymus (e.g. MTS1, CORO1A); (d) myasthenia gravis as the prototypic outcome of an inflamed or disordered neoplastic ‘sick thymus’.

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Keywords {🔍}

pubmed, article, google, scholar, cas, thymic, cells, central, thymus, aire, cell, immunol, autoimmune, myasthenia, expression, gravis, patients, human, epithelial, tcells, tolerance, mtecs, thymomas, development, regulatory, selection, autoantibodies, autoimmunity, httpsdoiorgs, marx, willcox, medulla, mice, bcells, medullary, apeced, gene, syndrome, mutations, genes, dcs, nat, tcell, receptor, sci, pvs, thymoma, exp, med, clin,

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skeletal muscle-derived achr/antibody-complexes phd-type zinc-finger domains amplify il-2r-stat5 signaling thymic cd19+cd5+cd1dhiil-10+ regulatory expressing mhc/achr-peptide complexes tlr-expressing antigen-presenting cells express mhc/achr-peptide complexes α/β-t-cell receptors autoreactive α/β-t-cells present mhcii/tra-peptide complexes article download pdf satb1-dependent super-enhancer establishment cd4+ t-cell-dependent haid elicit low-affinity antibodies aire-driven ins/insulin promoter achr-reactive t-cells occur nascent t-cells delivered anti-acetylcholine-receptor antibody fork head-related protein conventional hematoxylin-eosin stain �treg-specific demethylated region myoid cell-derived achrs promote central tolerance neoplastic aire-deficient clone immune system pre-programmed thymoproteasome-processed tra-peptides [28] live-cell imaging reveals regulate t-cell polarisation pre-emigrant t-cells [166] single aire-dependent tra cd4+ t-cell-dependent t-cell intrinsic factors polarity shape t-cell hematoxylin-eosin stain showing mhcii/tra peptide complexes march8-mediated mhcii turnover forkhead/winged-helix protein efficient antigen-presenting cells aire-expressing epithelial cells thymus-specific serine protease viral-specific plasma cells ltbetar-dependent thymocyte emigration α-myosin directs autoimmunity de moraes-pinto mi hc-deficient thymic rudiments epithelial-free perivascular space central immune tolerance antigen-presenting-cell subsets antigen-presenting cell subsets cell central tolerance

Questions {❓}

An expansion of a minor cortical epithelial cell subset?
James KD, Jenkinson WE, Anderson G (2018) T-cell egress from the thymus: should I stay or should I go?
Mortimer GL, Gillespie KM (2020) Early onset of autoimmune diabetes in children with Down syndrome-two separate aetiologies or an immune system pre-programmed for autoimmunity?
Zhao C, Rajan A (2019) Immune checkpoint inhibitors for treatment of thymic epithelial tumors: how to maximize benefit and optimize risk?

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         headline:Thymus and autoimmunity
         description:The thymus prevents autoimmune diseases through mechanisms that operate in the cortex and medulla, comprising positive and negative selection and the generation of regulatory T-cells (Tregs). Egress from the thymus through the perivascular space (PVS) to the blood is another possible checkpoint, as shown by some autoimmune/immunodeficiency syndromes. In polygenic autoimmune diseases, subtle thymic dysfunctions may compound genetic, hormonal and environmental cues. Here, we cover (a) tolerance-inducing cell types, whether thymic epithelial or tuft cells, or dendritic, B- or thymic myoid cells; (b) tolerance-inducing mechanisms and their failure in relation to thymic anatomic compartments, and with special emphasis on human monogenic and polygenic autoimmune diseases and the related thymic pathologies, if known; (c) polymorphisms and mutations of tolerance-related genes with an impact on positive selection (e.g. the gene encoding the thymoproteasome-specific subunit, PSMB11), promiscuous gene expression (e.g. AIRE, PRKDC, FEZF2, CHD4), Treg development (e.g. SATB1, FOXP3), T-cell migration (e.g. TAGAP) and egress from the thymus (e.g. MTS1, CORO1A); (d) myasthenia gravis as the prototypic outcome of an inflamed or disordered neoplastic ‘sick thymus’.
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      headline:Thymus and autoimmunity
      description:The thymus prevents autoimmune diseases through mechanisms that operate in the cortex and medulla, comprising positive and negative selection and the generation of regulatory T-cells (Tregs). Egress from the thymus through the perivascular space (PVS) to the blood is another possible checkpoint, as shown by some autoimmune/immunodeficiency syndromes. In polygenic autoimmune diseases, subtle thymic dysfunctions may compound genetic, hormonal and environmental cues. Here, we cover (a) tolerance-inducing cell types, whether thymic epithelial or tuft cells, or dendritic, B- or thymic myoid cells; (b) tolerance-inducing mechanisms and their failure in relation to thymic anatomic compartments, and with special emphasis on human monogenic and polygenic autoimmune diseases and the related thymic pathologies, if known; (c) polymorphisms and mutations of tolerance-related genes with an impact on positive selection (e.g. the gene encoding the thymoproteasome-specific subunit, PSMB11), promiscuous gene expression (e.g. AIRE, PRKDC, FEZF2, CHD4), Treg development (e.g. SATB1, FOXP3), T-cell migration (e.g. TAGAP) and egress from the thymus (e.g. MTS1, CORO1A); (d) myasthenia gravis as the prototypic outcome of an inflamed or disordered neoplastic ‘sick thymus’.
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