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  • 1
    Online-Ressource
    Online-Ressource
    IL ‐13 R α1 is a surface marker for M 2 macrophages influencing their differentiation and function
    Wiley ; 2014
    In:  European Journal of Immunology Vol. 44, No. 3 ( 2014-03), p. 842-855
    Details
    In: European Journal of Immunology, Wiley, Vol. 44, No. 3 ( 2014-03), p. 842-855
    Kurzfassung: In this study, we examined the role IL ‐13 receptor alpha 1 ( IL ‐13 R α1) plays in macrophage differentiation and function. The findings indicate that IL ‐13 R α1 is expressed on the M 2 but not on the M 1 subset of macrophages and specifically heterodimerizes with the IL ‐4 R α chain to form a type II receptor, which controls the differentiation and function of these cells. Indeed, BM cells from IL ‐13 R α1 +/+ and IL ‐13 R α1 −/− mice yield equivalent numbers of macrophages when cultured under M 2 polarizing conditions. However, IL ‐13 R α1 −/− BM cells yield a much higher number of macrophages than IL ‐13 R α1 +/+ BM cells when the differentiation is carried out under M 1‐polarizing conditions. Further analyses indicated that macrophages that express IL ‐13 R α1 also display surface markers associated with an M 2 phenotype. In addition, the IL ‐13 R α1 + macrophages were highly efficient in phagocytizing zymosan bioparticles both in vitro and in vivo, and supported differentiation of naïve T cells to a T h2 phenotype. Finally, when stimulated by IL ‐13, a cytokine that uses the heteroreceptor, the cells were able to phosphorylate STAT 6 efficiently. These previously unrecognized findings indicate that IL ‐13 R α1 serves as a marker for M 2 macrophages and the resulting heteroreceptor influences both their differentiation and function.
    Materialart: Online-Ressource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    URL: Article
    DOI: 10.1002/eji.v44.3
    DOI: 10.1002/eji.201343755
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2014
    ZDB Id: 1491907-2
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Online-Ressource
    Online-Ressource
    Bone Marrow-Derived IL-13Rα1–Positive Thymic Progenitors Are Restricted to the Myeloid Lineage
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 7 ( 2012-04-01), p. 3208-3216
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 7 ( 2012-04-01), p. 3208-3216
    Kurzfassung: The earliest thymic progenitors (ETPs) were recently shown to give rise to both lymphoid and myeloid cells. Whereas the majority of ETPs are derived from IL-7Rα–positive cells and give rise exclusively to T cells, the origin of the myeloid cells remains undefined. In this study, we show both in vitro and in vivo that IL-13Rα1+ ETPs yield myeloid cells with no potential for maturation into T cells, whereas IL-13Rα1− ETPs lack myeloid potential. Moreover, transfer of lineage-negative IL-13Rα1+ bone marrow stem cells into IL-13Rα1–deficient mice reconstituted thymic IL-13Rα1+ myeloid ETPs. Myeloid cells or macrophages in the thymus are regarded as phagocytic cells whose function is to clear apoptotic debris generated during T cell development. However, the myeloid cells derived from IL-13Rα1+ ETPs were found to perform Ag-presenting functions. Thus, IL-13Rα1 defines a new class of myeloid restricted ETPs yielding APCs that could contribute to development of T cells and the control of immunity and autoimmunity.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1103316
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2012
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    Online-Ressource
    Online-Ressource
    Developmental Expression of IL-12Rβ2 on Murine Naive Neonatal T Cells Counters the Upregulation of IL-13Rα1 on Primary Th1 Cells and Balances Immunity in the Newborn
    The American Association of Immunologists ; 2013
    In:  The Journal of Immunology Vol. 190, No. 12 ( 2013-06-15), p. 6155-6163
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 190, No. 12 ( 2013-06-15), p. 6155-6163
    Kurzfassung: Upon exposure to Ag on the day of birth, neonatal mice mount balanced primary Th1 and Th2 responses, with the former displaying upregulated IL-13Rα1 expression. This chain associates with IL-4Rα to form a heteroreceptor (IL-4Rα/IL-13Rα1) that marks the Th1 cells for death by IL-4 produced by Th2 cells during rechallenge with Ag, hence the Th2 bias of murine neonatal immunity. The upregulation of IL-13Rα1 on neonatal Th1 cells was due to the paucity of IL-12 in the neonatal environment. In this study, we show that by day 8 after birth, naive splenic T cells are no longer susceptible to IL-13Rα1 upregulation even when exposed to Ag within the neonatal environment. Furthermore, during the 8-d lapse, the naive splenic T cells spontaneously and progressively upregulate the IL-12Rβ2 chain, perhaps due to colonization by commensals, which induce production of IL-12 by cells of the innate immune system such as dendritic cells. In fact, mature T cells from the thymus, a sterile environment not accessible to microbes, did not upregulate IL-12Rβ2 and were unable to counter IL-13Rα1 upregulation. Finally, the 8-d naive T cells were able to differentiate into Th1 cells even independently of IL-12 but required the cytokine to counter upregulation of IL-13Rα1. Thus, in neonatal mice, IL-12, which accumulates in the environment progressively, uses IL-12Rβ2 to counter IL-13Rα1 expression in addition to promoting Th1 differentiation.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1202207
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2013
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Online-Ressource
    Online-Ressource
    Recovery From Overt Type 1 Diabetes Ensues When Immune Tolerance and β-Cell Formation Are Coupled With Regeneration of Endothelial Cells in the Pancreatic Islets
    American Diabetes Association ; 2013
    In:  Diabetes Vol. 62, No. 8 ( 2013-08-01), p. 2879-2889
    Details
    In: Diabetes, American Diabetes Association, Vol. 62, No. 8 ( 2013-08-01), p. 2879-2889
    Kurzfassung: Immune modulation of pancreatic inflammation induces recovery from type 1 diabetes (T1D), but remission was not durable, perhaps because of an inability to sustain the formation and function of new pancreatic β-cells. We have previously shown that Ig-GAD2, carrying GAD 206–220 peptide, induced in hyperglycemic mice immune modulation that was able to control pancreatic inflammation, stimulate β-cell regeneration, and prevent T1D progression. Herein, we show that the same Ig-GAD2 regimen given to mice with overt T1D was unable to reverse the course of disease despite eradication of Th1 and Th17 cells from the pancreas. However, the regimen was able to sustain recovery from T1D when Ig-GAD2 was accompanied with transfer of bone marrow (BM) cells from healthy donors. Interestingly, alongside immune modulation, there was concomitant formation of new β-cells and endothelial cells (ECs) in the pancreas. The new β-cells were of host origin while the donor BM cells gave rise to the ECs. Moreover, transfer of purified BM endothelial progenitors instead of whole BM cells sustained both β-cell and EC formation and reversal of diabetes. Thus, overcoming T1D requires both immune modulation and repair of the islet vascular niche to preserve newly formed β-cells.
    Materialart: Online-Ressource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db12-1281
    Sprache: Englisch
    Verlag: American Diabetes Association
    Publikationsdatum: 2013
    ZDB Id: 1501252-9
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    Online-Ressource
    Online-Ressource
    Delayed maturation of an IL-12–producing dendritic cell subset explains the early Th2 bias in neonatal immunity
    Rockefeller University Press ; 2008
    In:  The Journal of Experimental Medicine Vol. 205, No. 10 ( 2008-09-29), p. 2269-2280
    Details
    In: The Journal of Experimental Medicine, Rockefeller University Press, Vol. 205, No. 10 ( 2008-09-29), p. 2269-2280
    Kurzfassung: Primary neonatal T cell responses comprise both T helper (Th) cell subsets, but Th1 cells express high levels of interleukin 13 receptor α1 (IL-13Rα1), which heterodimerizes with IL-4Rα. During secondary antigen challenge, Th2-produced IL-4 triggers the apoptosis of Th1 cells via IL-4Rα/IL-13Rα1, thus explaining the Th2 bias in neonates. We show that neonates acquire the ability to overcome the Th2 bias and generate Th1 responses starting 6 d after birth. This transition was caused by the developmental maturation of CD8α+CD4− dendritic cells (DCs), which were minimal in number during the first few days of birth and produced low levels of IL-12. This lack of IL-12 sustained the expression of IL-13Rα1 on Th1 cells. By day 6 after birth, however, a significant number of CD8α+CD4− DCs accumulated in the spleen and produced IL-12, which triggered the down-regulation of IL-13Rα1 expression on Th1 cells, thus protecting them against IL-4–driven apoptosis.
    Materialart: Online-Ressource
    ISSN: 1540-9538 , 0022-1007
    URL: Article
    DOI: 10.1084/jem.20071371
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Rockefeller University Press
    Publikationsdatum: 2008
    ZDB Id: 1477240-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
    Online-Ressource
    Online-Ressource
    APCs Expressing High Levels of Programmed Death Ligand 2 Sustain the Development of CD4 T Cell Memory
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 185, No. 6 ( 2010-09-15), p. 3149-3157
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 185, No. 6 ( 2010-09-15), p. 3149-3157
    Kurzfassung: The role APCs play in the transition of T cells from effector to memory remains largely undefined. This is likely due to the low frequency at which long-lived T cells arise, which hinders analysis of the events involved in memory development. In this study, we used TCR transgenic T cells to increase the frequency of long-lived T cells and developed a transfer model suitable for defining the contribution of APCs to the development of CD4 T cell memory. Accordingly, naive TCR transgenic T cells were stimulated in vitro with Ag presented by different types of APCs and transferred into MHC class II-deficient mice for parking, and the hosts were later analyzed for long-lived T cell frequency or challenged with suboptimal dose of Ag, and the long-lived cells-driven memory responses were measured. The findings indicate that B cells and CD8α+ dendritic cells sustained elevated frequencies of long-lived T cells that yielded rapid and robust memory responses upon rechallenge with suboptimal dose of Ag. Furthermore, both types of APCs had significant programmed death (PD) ligand 2 expression prior to Ag stimulation, which was maintained at a high level during presentation of Ag to T cells. Blockade of PD ligand 2 interaction with its receptor PD-1 nullified the development of memory responses. These previously unrecognized findings suggest that targeting specific APCs for Ag presentation during vaccination could prove effective against microbial infections.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1000810
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2010
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
    Online-Ressource
    Online-Ressource
    FoxP3+RORγt+ T Helper Intermediates Display Suppressive Function against Autoimmune Diabetes
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 7 ( 2010-04-01), p. 3377-3385
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 7 ( 2010-04-01), p. 3377-3385
    Kurzfassung: Recently, traces of double-positive FoxP3+RORγt+ T cells were identified and viewed as dual programming differentiation intermediates geared toward development into T regulatory or Th17 cells. In this study, we report that FoxP3+RORγt+ intermediates arise in the NOD mouse T cell repertoire prior to inflammation and can be expanded with tolerogen without further differentiation. Furthermore, FoxP3+RORγt+ cells express both CD62L and membrane-bound TGFβ and use the former to traffic to the pancreas and the latter to suppress effector T cells both in vitro and in vivo. The cells perform these functions as FoxP3+RORγt+ intermediates, despite being able to terminally differentiate into either FoxP3+RORγt− T regulatory or FoxP3−RORγt+ Th17 cells on polarization. These previously unrecognized observations extend plasticity to both differentiation and function and indicate that the intermediates are poised to traffic to sites of inflammation and target diverse pathogenic T cells, likely without prior conditioning by effector T cells, thus broadening efficacy against autoimmunity.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.0903324
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2010
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
    Online-Ressource
    Online-Ressource
    Antigen-Free Adjuvant Assists Late Effector CD4 T Cells To Transit to Memory in Lymphopenic Hosts
    The American Association of Immunologists ; 2013
    In:  The Journal of Immunology Vol. 191, No. 3 ( 2013-08-01), p. 1126-1135
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 191, No. 3 ( 2013-08-01), p. 1126-1135
    Kurzfassung: The events controlling the transition of T cells from effector to memory remain largely undefined. Many models have been put forth to account for the origin of memory precursors, but for CD4 T cells initial studies reported that memory T cells derive from IFN-γ–nonproducing effectors, whereas others suggested that memory emanates from highly activated IFN-γ–producing effectors. In this study, using cell proliferation, expression of activation markers, and production of IFN-γ as a measure of activation, we defined two types of effector CD4 T cells and investigated memory generation. The moderately activated early effectors readily transit to memory, whereas the highly activated late effectors, regardless of their IFN-γ production, develop minimal memory. Boosting with Ag-free adjuvant, however, rescues late effectors from cell death and sustains both survival and IFN-γ cytokine responses in lymphopenic hosts. The adjuvant-mediated memory transition of late effectors involves the function of TLRs, most notably TLR9. These findings uncover the mechanism by which late effector CD4 T cells are driven to transit to memory and suggest that timely boosts with adjuvant may enhance vaccine efficacy.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1202262
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2013
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
    Online-Ressource
    Online-Ressource
    In Trans T Cell Tolerance Diminishes Autoantibody Responses and Exacerbates Experimental Allergic Encephalomyelitis
    The American Association of Immunologists ; 2008
    In:  The Journal of Immunology Vol. 180, No. 3 ( 2008-02-01), p. 1508-1516
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 180, No. 3 ( 2008-02-01), p. 1508-1516
    Kurzfassung: A number of Ag-specific approaches have been developed that ameliorate experimental allergic encephalomyelitis (EAE), an animal model for the human autoimmune disease multiple sclerosis. Translation to humans, however, remains a consideration, justifying the search for more insight into the mechanism underlying restoration of self-tolerance. Ig-proteolipid protein (PLP) 1 and Ig-myelin oligodendrocyte glycoprotein (MOG) are Ig chimeras carrying the encephalitogenic PLP 139–151 and MOG 35–55 amino acid sequence, respectively. Ig-PLP1 ameliorates EAE in SJL/J (H-2s) mice while Ig-MOG modulates the disease in C57BL/6 (H-2b) animals. In this study, we asked whether the chimeras would suppress EAE in F1 mice expressing both parental MHC alleles and representing a polymorphism with more relevance to human circumstances. The results show that Ig-MOG modulates both PLP1 and MOG peptide-induced EAE in the F1 mice, whereas Ig-PLP1 counters PLP1 EAE but exacerbates MOG-induced disease. This in trans aggravation of MOG EAE by Ig-PLP1 operates through induction of PLP1-specific T cells producing IL-5 that sustained inhibition of MOG-specific Abs leading to exacerbation of EAE. Thus, in trans T cell tolerance, which should be operative in polymorphic systems, can aggravate rather than ameliorate autoimmunity. This phenomenon possibly takes place through interference with protective humoral immunity.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.180.3.1508
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2008
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
    Online-Ressource
    Online-Ressource
    A New IRF-1–Driven Apoptotic Pathway Triggered by IL-4/IL-13 Kills Neonatal Th1 Cells and Weakens Protection against Viral Infection
    The American Association of Immunologists ; 2019
    In:  The Journal of Immunology Vol. 202, No. 11 ( 2019-06-01), p. 3173-3186
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 202, No. 11 ( 2019-06-01), p. 3173-3186
    Kurzfassung: Early life immune responses are deficient in Th1 lymphocytes that compromise neonatal vaccination. We found that IL-4 and IL-13 engage a developmentally expressed IL-4Rα/IL-13Rα1 heteroreceptor to endow IFN regulatory factor 1 (IRF-1) with apoptotic functions, which redirect murine neonatal Th1 reactivation to cell death. IL-4/IL-13–induced STAT6 phosphorylation serves to enhance IRF-1 transcription and promotes its egress from the nucleus. In the cytoplasm, IRF-1 can no longer serve as an anti-viral transcription factor but, instead, colocalizes with Bim and instigates the mitochondrial, or intrinsic, death pathway. The new pivotal function of IRF-1 in the death of neonatal Th1 cells stems from the ability of its gene to bind STAT6 for enhanced transcription and the proficiency of its protein to precipitate Bim-driven apoptosis. This cytokine-induced, IRF-1–mediated developmental death network weakens neonatal Th1 responses during early life vaccination and increases susceptibility to viral infection.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1800943
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2019
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
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