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  • 1
    Online Resource
    Online Resource
    Cham :Springer International Publishing AG,
    Keywords: Immunologic diseases--Alternative treatment. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (123 pages)
    Edition: 1st ed.
    ISBN: 9783319645261
    Series Statement: Current Topics in Microbiology and Immunology Series ; v.408
    DDC: 616.97059999999999
    Language: English
    Note: Intro -- Preface -- References -- Contents -- 22 The Appearance and Diversification of Receptors for IgM During Vertebrate Evolution -- Abstract -- 1 The Adaptive Immune System of Vertebrates -- 2 The Appearance of Receptors Interacting with the Constant Domain of Igs -- 3 The Polymeric Ig Receptor-PIGR -- 4 The FcαµR -- 5 The FcµR -- 6 Concluding Remarks -- Acknowledgements -- References -- 23 Authentic IgM Fc Receptor (FcμR) -- Abstract -- 1 Introduction -- 2 Lymphocyte-Restricted Expression of FcµR -- 3 Unique Ligand-Binding Activity -- 3.1 Fcµ-Specificity, Ligand-Binding Avidity, and Glycosylation -- 3.2 Cis Engagement -- 3.3 Modulatory Effect of FcµR by Cis Engagement -- 3.4 Key Residues in the Transmembrane and Cytoplasmic Tail for FcµR Function -- 4 FcµR Deficiency in Mice -- 5 Epilogue -- Acknowledgements -- References -- 40 FCRLA-A Resident Endoplasmic Reticulum Protein that Associates with Multiple Immunoglobulin Isotypes in B Lineage Cells -- Abstract -- 1 Introduction-Fc Receptors and Their Relatives -- 2 The Identification of FCRLA and FCRLB -- 3 The FCRLA Genome Landscape -- 4 Features of the FCRLA Protein -- 5 FCRLA-Phylogeny and Disease Association -- 6 FCRLA-Expression Pattern and Regulation -- 7 FCRLA is a Soluble Resident ER Protein -- 8 FCRLA is Retained in the ER via its N-terminal Disordered Domain -- 9 FCRLA Associates with Multiple Ig Isotypes in the ER -- 10 TRIM21-One Other Intracellular Fc Receptor that Binds Multiple Ig Isotypes -- 11 FCRLA Function-Facts and Speculations -- 11.1 Facts -- 11.2 Speculations -- Acknowledgements -- References -- 24 Specific IgM and Regulation of Antibody Responses -- Abstract -- 1 Introduction -- 1.1 IgG-Mediated Feedback Suppression -- 1.2 IgG-Mediated Feedback Enhancement -- 1.3 IgE-Mediated Feedback Enhancement -- 1.4 IgM-Mediated Feedback Enhancement. , 2 Basic Parameters of IgM-Mediated Enhancement -- 2.1 Antigens -- 2.2 The IgM Molecule and Mode of Administration -- 2.3 Primary Antibody Responses -- 2.4 Priming for Memory Responses -- 2.5 Avidity of the Enhanced Response -- 2.6 Germinal Center Responses -- 2.7 Specificity of the Enhanced Antibody Response -- 2.8 T Cells and IgM-Mediated Enhancement -- 3 Complement in Antibody Responses to Uncomplexed Antigen -- 4 Complement in Antibody Responses to IgM-Antigen Complexes -- 4.1 Complement Activation by IgM -- 4.2 Complement Receptors 1 and 2, CR1/2, in Antibody Responses to IgM-Antigen Complexes -- 4.3 Cμ13 Knock-in Mice with a Point Mutation in the IgM Heavy Chain Abolishing C1q-Binding -- 4.4 FcμR (Toso/Faim3) and IgM-Mediated Enhancement -- 4.5 Other IgM-Binding Receptors and IgM-Mediated Enhancement -- 4.6 Specific IgM from Wildtype but not Cμ13 Mice, Causes Rapid Deposition of C3 on SRBC in Vivo -- 5 Transport of IgM-Antigen Complexes to Splenic B Cell Follicles -- 6 Summary and Concluding Discussion -- References -- 37 Role of Natural IgM Autoantibodies (IgM-NAA) and IgM Anti-Leukocyte Antibodies (IgM-ALA) in Regulating Inflammation -- Abstract -- 1 Introduction -- 2 Natural Autoantibodies and B1 Cells -- 3 Physiological Role of IgM-NAA -- 4 Physiologic Role of IgM-ALA in Regulating Inflammation -- 4.1 B Cell Clones Obtained from Human Umbilical Cord Produce IgM-ALA that Exhibit Leukocyte Receptor Specificity-Binding of IgM to Leukocytes Was not Mediated by FcμR -- 4.2 IgM-ALA from Different Human Sera Differ in Their Repertoire for Receptor Binding. IgM Regulates Human T Effector Cells and DC Without Affecting Tregs or Chemokine Production -- 4.3 The Function of Murine T Effector Cells, DC and NKT Cells but not Tregs Is Regulated by Binding of Polyclonal IgM to Specific Co-Stimulatory Receptors. , 4.4 Innate Immune Inflammatory Response in Renal Ischemia Reperfusion Injury (IRI) Is Inhibited by IgM-ALA -- 4.5 Ex Vivo Induced Regulatory DC Are Protective in Renal Ischemia. Regulatory DC Require Tregs, B Cells, Circulating IgM and IL10 to Mediate in vivo Protection -- 4.6 Inflammation Mediated by Adaptive Immune Mechanisms in Allograft Transplantation Is Inhibited by Polyclonal IgM -- 4.7 Autoimmune-Mediated Insulitis in NOD Mice Is Inhibited by Polyclonal IgM -- 5 Pathogenic Effects of IgM-NAA Under Non-physiological Conditions -- 6 Conclusion -- References.
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 764 (1995), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: Newfound relatives of the classical Fc receptors (FcR) have been provisionally named the Fc receptor homologs (FcRH). The recent identification of eight human and six mouse FcRH genes substantially increases the size and functional potential of the FcR family. The extended family of FcR and FcRH genes spans ∼15 Mb of the human chromosome 1q21–23 region, whereas in mice this family is split between chromosomes 1 and 3. The FcRH genes encode molecules with variable combinations of five subtypes of immunoglobulin (Ig) domains. The presence of a conserved sequence motif in one Ig domain subtype implies Ig Fc binding capability for many FcRH family members that are preferentially expressed by B lineage cells. In addition, most FcRH family members have consensus tyrosine-based activating and inhibitory motifs in their cytoplasmic domains, while the others lack features typical of transmembrane receptors. The FcRH family members, like the classical FcRs, come in multiple isoforms and allelic variations. The unique individual and polymorphic properties of the FcR/FcRH members indicate a remarkably diverse Fc receptor gene family with immunoregulatory function.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK; Malden , USA : Blackwell Publishing Ltd/Inc
    Immunological reviews 197 (2004), S. 0 
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary:  First observed in mouse pre-B-cell lines and then in knock-in mice carrying self-reactive IgH transgenes, VH replacement has now been shown to contribute to the primary B-cell repertoire in humans. Through recombination-activating gene (RAG)-mediated recombination between a cryptic recombination signal sequence (RSS) present in almost all VH genes and the flanking 23 base pair RSS of an upstream VH gene, VH replacement renews the entire VH-coding region, while leaving behind a short stretch of nucleotides as a VH replacement footprint. In addition to extending the CDR3 region, the VH replacement footprints preferentially contribute charged amino acids. VH replacement rearrangement in immature B cells may either eliminate a self-reactive B-cell receptor or contribute to the generation of self-reactive antibodies. VH replacement may also rescue non-productive or dysfunctional VHDJH rearrangement in pro-B and pre-B cells. Conversely, VH replacement of a productive immunoglobulin H gene may generate non-productive VH replacement to disrupt or temporarily reverse the B-cell differentiation process. VH replacement can thus play a complex role in the generation of the primary B-cell repertoire.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Figure 1 shows an unequal sister chromatid exchange mechanism and the predicted genotypes of the progeny cells which would be produced in cell line 18-81. The two different V alleles of 18-81 are designated V2 and V3 because they contain J2 and J3, respectively8,9. The silent allele is V2, the ...
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 306 (1983), S. 243-246 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Switching of an Abelson virus-transformed mouse lymphoid cell line from immunoglobulin μ to γ2b heavy-chain synthesis in vitro is accompanied by loss of DNA sequences between the JH and Cγ2b gene segments, and thus cannot be explained by differential RNA ...
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 63 (1984), S. 97-111 
    ISSN: 1573-4919
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Conclusions While much has been learned concerning the molecular structural basis for the heavy chain class switch, many questions relating to the regulation of the switch remain unanswered, or at least controversial. Identification of the enzyme system which mediates the class switch, as well as other regulatory, possibly X-linked, genes should provide the necessary key to our understanding of this unique process.
    Type of Medium: Electronic Resource
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