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Article ; Online: BAFFR controls early memory B cell responses but is dispensable for germinal center function.

Lau, Angelica W Y / Turner, Vivian M / Bourne, Katherine / Hermes, Jana R / Chan, Tyani D / Brink, Robert

2020 Volume 218, Issue 2

Abstract: The TNF superfamily ligand BAFF maintains the survival of naive B cells by signaling through its surface receptor, BAFFR. Activated B cells maintain expression of BAFFR after they differentiate into germinal center (GC) or memory B cells (MBCs). However, ...

Abstract	The TNF superfamily ligand BAFF maintains the survival of naive B cells by signaling through its surface receptor, BAFFR. Activated B cells maintain expression of BAFFR after they differentiate into germinal center (GC) or memory B cells (MBCs). However, the functions of BAFFR in these antigen-experienced B cell populations remain unclear. Here, we show that B cell-intrinsic BAFFR does not play a significant role in the survival or function of GC B cells or in the generation of the somatically mutated MBCs derived from them. Instead, BAFF/BAFFR signaling was required to generate the unmutated, GC-independent MBCs that differentiate directly from activated B cell blasts early in the response. Furthermore, amplification of BAFFR signaling in responding B cells did not affect GCs or the generation of GC-derived MBCs but greatly expanded the GC-independent MBC response. Although BAFF/BAFFR signaling specifically controlled the formation of the GC-independent MBC response, both types of MBCs required input from this pathway for optimal long-term survival.
MeSH term(s)	Animals ; B-Cell Activating Factor/immunology ; B-Cell Activating Factor/metabolism ; B-Cell Activation Factor Receptor/immunology ; B-Cell Activation Factor Receptor/metabolism ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Germinal Center/immunology ; Germinal Center/metabolism ; Immunologic Memory/immunology ; Mice ; Mice, Inbred C57BL ; Signal Transduction/physiology
Chemical Substances	B-Cell Activating Factor ; B-Cell Activation Factor Receptor ; Tnfrsf13c protein, mouse
Language	English
Publishing date	2020-11-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20191167
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Ua VI Zs.107: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Positive selection of IgG

Sundling, Christopher / Lau, Angelica W Y / Bourne, Katherine / Young, Clara / Laurianto, Candy / Hermes, Jana R / Menzies, Rosemary J / Butt, Danyal / Kräutler, Nike J / Zahra, David / Suan, Dan / Brink, Robert

Immunity

2021 Volume 54, Issue 5, Page(s) 988–1001.e5

Abstract: Positive selection of high-affinity B cells within germinal centers (GCs) drives affinity maturation of antibody responses. Here, we examined the mechanism underlying the parallel transition from immunoglobulin M (IgM) to IgG. Early GCs contained mostly ... ...

Abstract	Positive selection of high-affinity B cells within germinal centers (GCs) drives affinity maturation of antibody responses. Here, we examined the mechanism underlying the parallel transition from immunoglobulin M (IgM) to IgG. Early GCs contained mostly unswitched IgM
MeSH term(s)	Animals ; Antibody Formation/immunology ; Antigens/immunology ; B-Lymphocytes/immunology ; Female ; Germinal Center/immunology ; Immunoglobulin Class Switching/immunology ; Immunoglobulin G/immunology ; Immunoglobulin M/immunology ; Immunoglobulin Variable Region/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Sheep/immunology ; Somatic Hypermutation, Immunoglobulin/immunology
Chemical Substances	Antigens ; Immunoglobulin G ; Immunoglobulin M ; Immunoglobulin Variable Region
Language	English
Publishing date	2021-04-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2021.03.013
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Germinal center antibody mutation trajectories are determined by rapid self/foreign discrimination.

Burnett, Deborah L / Langley, David B / Schofield, Peter / Hermes, Jana R / Chan, Tyani D / Jackson, Jennifer / Bourne, Katherine / Reed, Joanne H / Patterson, Kate / Porebski, Benjamin T / Brink, Robert / Christ, Daniel / Goodnow, Christopher C

Science (New York, N.Y.)

2018 Volume 360, Issue 6385, Page(s) 223–226

Abstract: Antibodies have the specificity to differentiate foreign antigens that mimic self antigens, but it remains unclear how such specificity is acquired. In a mouse model, we generated B cells displaying an antibody that cross-reacts with two related protein ... ...

Abstract	Antibodies have the specificity to differentiate foreign antigens that mimic self antigens, but it remains unclear how such specificity is acquired. In a mouse model, we generated B cells displaying an antibody that cross-reacts with two related protein antigens expressed on self versus foreign cells. B cell anergy was imposed by self antigen but reversed upon challenge with high-density foreign antigen, leading to germinal center recruitment and antibody gene hypermutation. Single-cell analysis detected rapid selection for mutations that decrease self affinity and slower selection for epistatic mutations that specifically increase foreign affinity. Crystal structures revealed that these mutations exploited subtle topological differences to achieve 5000-fold preferential binding to foreign over self epitopes. Resolution of antigenic mimicry drove the optimal affinity maturation trajectory, highlighting the value of retaining self-reactive clones as substrates for protective antibody responses.
MeSH term(s)	Animals ; Antibodies/chemistry ; Antibodies/genetics ; Antibodies/immunology ; Antibody Affinity/genetics ; Antibody Formation/genetics ; Autoantigens/immunology ; B-Lymphocytes/immunology ; Clonal Anergy ; Cross Reactions ; Crystallography, X-Ray ; Germinal Center/immunology ; Mice ; Mice, Mutant Strains ; Molecular Mimicry/genetics ; Mutation ; Nucleoproteins/genetics ; Nucleoproteins/immunology ; Selection, Genetic ; Self Tolerance ; Single-Cell Analysis
Chemical Substances	Antibodies ; Autoantigens ; Nucleoproteins ; peptide 31D (122289-52-5)
Language	English
Publishing date	2018-05-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.aao3859
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Zs.A 27: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: CCR6 Defines Memory B Cell Precursors in Mouse and Human Germinal Centers, Revealing Light-Zone Location and Predominant Low Antigen Affinity.

Suan, Dan / Kräutler, Nike J / Maag, Jesper L V / Butt, Danyal / Bourne, Katherine / Hermes, Jana R / Avery, Danielle T / Young, Clara / Statham, Aaron / Elliott, Michael / Dinger, Marcel E / Basten, Antony / Tangye, Stuart G / Brink, Robert

Immunity

2017 Volume 47, Issue 6, Page(s) 1142–1153.e4

Abstract: Memory B cells (MBCs) and plasma cells (PCs) constitute the two cellular outputs of germinal center (GC) responses that together facilitate long-term humoral immunity. Although expression of the transcription factor BLIMP-1 identifies cells undergoing PC ...

Abstract	Memory B cells (MBCs) and plasma cells (PCs) constitute the two cellular outputs of germinal center (GC) responses that together facilitate long-term humoral immunity. Although expression of the transcription factor BLIMP-1 identifies cells undergoing PC differentiation, no such marker exists for cells committed to the MBC lineage. Here, we report that the chemokine receptor CCR6 uniquely marks MBC precursors in both mouse and human GCs. CCR6
MeSH term(s)	Animals ; B7-2 Antigen/genetics ; B7-2 Antigen/immunology ; Cell Differentiation ; Cell Lineage/immunology ; Gene Expression Profiling ; Gene Expression Regulation ; Germinal Center/cytology ; Germinal Center/immunology ; Humans ; Immunity, Humoral ; Immunologic Memory ; Immunophenotyping ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Phenotype ; Plasma Cells/cytology ; Plasma Cells/immunology ; Positive Regulatory Domain I-Binding Factor 1/genetics ; Positive Regulatory Domain I-Binding Factor 1/immunology ; Precursor Cells, B-Lymphoid/cytology ; Precursor Cells, B-Lymphoid/immunology ; Receptors, CCR6/genetics ; Receptors, CCR6/immunology ; Receptors, CXCR4/genetics ; Receptors, CXCR4/immunology ; Signal Transduction
Chemical Substances	B7-2 Antigen ; CCR6 protein, mouse ; CXCR4 protein, mouse ; Cd86 protein, mouse ; Prdm1 protein, mouse ; Receptors, CCR6 ; Receptors, CXCR4 ; Positive Regulatory Domain I-Binding Factor 1 (EC 2.1.1.-)
Language	English
Publishing date	2017--19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2017.11.022
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Differentiation of germinal center B cells into plasma cells is initiated by high-affinity antigen and completed by Tfh cells.

Kräutler, Nike J / Suan, Dan / Butt, Danyal / Bourne, Katherine / Hermes, Jana R / Chan, Tyani D / Sundling, Christopher / Kaplan, Warren / Schofield, Peter / Jackson, Jennifer / Basten, Antony / Christ, Daniel / Brink, Robert

The Journal of experimental medicine

2017 Volume 214, Issue 5, Page(s) 1259–1267

Abstract: Plasma cells (PCs) derived from germinal centers (GCs) secrete the high-affinity antibodies required for long-term serological immunity. Nevertheless, the process whereby GC B cells differentiate into PCs is uncharacterized, and the mechanism underlying ... ...

Abstract	Plasma cells (PCs) derived from germinal centers (GCs) secrete the high-affinity antibodies required for long-term serological immunity. Nevertheless, the process whereby GC B cells differentiate into PCs is uncharacterized, and the mechanism underlying the selective PC differentiation of only high-affinity GC B cells remains unknown. In this study, we show that differentiation into PCs is induced among a discrete subset of high-affinity B cells residing within the light zone of the GC. Initiation of differentiation required signals delivered upon engagement with intact antigen. Signals delivered by T follicular helper cells were not required to initiate differentiation but were essential to complete the differentiation process and drive migration of maturing PCs through the dark zone and out of the GC. This bipartite or two-signal mechanism has likely evolved to both sustain protective immunity and avoid autoantibody production.
MeSH term(s)	Animals ; Antigens, Differentiation, B-Lymphocyte/physiology ; B-Lymphocytes/physiology ; Cell Differentiation/physiology ; Germinal Center/physiology ; Mice ; Mice, Inbred C57BL ; Plasma Cells/physiology ; T-Lymphocytes, Helper-Inducer/physiology
Chemical Substances	Antigens, Differentiation, B-Lymphocyte
Language	English
Publishing date	2017-03-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20161533
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Ua VI Zs.107: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Elimination of germinal-center-derived self-reactive B cells is governed by the location and concentration of self-antigen.

Chan, Tyani D / Wood, Katherine / Hermes, Jana R / Butt, Danyal / Jolly, Christopher J / Basten, Antony / Brink, Robert

Immunity

2012 Volume 37, Issue 5, Page(s) 893–904

Abstract: Secondary diversification of the B cell repertoire by immunoglobulin gene somatic hypermutation in the germinal center (GC) is essential for providing the high-affinity antibody specificities required for long-term humoral immunity. While the risk to ... ...

Abstract	Secondary diversification of the B cell repertoire by immunoglobulin gene somatic hypermutation in the germinal center (GC) is essential for providing the high-affinity antibody specificities required for long-term humoral immunity. While the risk to self-tolerance posed by inadvertent generation of self-reactive GC B cells has long been recognized, it has not previously been possible to identify such cells and study their fate. In the current study, self-reactive B cells generated de novo in the GC failed to survive when their target self-antigen was either expressed ubiquitously or specifically in cells proximal to the GC microenvironment. By contrast, GC B cells that recognized rare or tissue-specific self-antigens were not eliminated, and could instead undergo positive selection by cross-reactive foreign antigen and produce plasma cells secreting high-affinity autoantibodies. These findings demonstrate the incomplete nature of GC self-tolerance and may explain the frequent association of cross-reactive, organ-specific autoantibodies with postinfectious autoimmune disease.
MeSH term(s)	Animals ; Antibody Affinity/genetics ; Antibody Affinity/immunology ; Autoantigens/genetics ; Autoantigens/immunology ; Autoantigens/metabolism ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; CHO Cells ; Cell Line ; Cellular Microenvironment/genetics ; Cellular Microenvironment/immunology ; Cricetinae ; Cross Reactions ; Genes, Immunoglobulin ; Germinal Center/immunology ; Germinal Center/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Plasma Cells/immunology ; Plasma Cells/metabolism ; Somatic Hypermutation, Immunoglobulin/genetics ; Somatic Hypermutation, Immunoglobulin/immunology
Chemical Substances	Autoantigens
Language	English
Publishing date	2012-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2012.07.017
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Memory B cells are reactivated in subcapsular proliferative foci of lymph nodes.

Nature communications

2018 Volume 9, Issue 1, Page(s) 3372

Abstract: Vaccine-induced immunity depends on the generation of memory B cells (MBC). However, where and how MBCs are reactivated to make neutralising antibodies remain unknown. Here we show that MBCs are prepositioned in a subcapsular niche in lymph nodes where, ... ...

Abstract	Vaccine-induced immunity depends on the generation of memory B cells (MBC). However, where and how MBCs are reactivated to make neutralising antibodies remain unknown. Here we show that MBCs are prepositioned in a subcapsular niche in lymph nodes where, upon reactivation by antigen, they rapidly proliferate and differentiate into antibody-secreting plasma cells in the subcapsular proliferative foci (SPF). This novel structure is enriched for signals provided by T follicular helper cells and antigen-presenting subcapsular sinus macrophages. Compared with contemporaneous secondary germinal centres, SPF have distinct single-cell molecular signature, cell migration pattern and plasma cell output. Moreover, SPF are found both in human and mouse lymph nodes, suggesting that they are conserved throughout mammalian evolution. Our data thus reveal that SPF is a seat of immunological memory that may be exploited to rapidly mobilise secondary antibody responses and improve vaccine efficacy.
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; CD4-Positive T-Lymphocytes/metabolism ; Cell Movement/drug effects ; Cells, Cultured ; Flow Cytometry ; Humans ; Lymph Nodes/immunology ; Lymph Nodes/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Theoretical ; Pyrazoles/pharmacology ; Pyrimidines/pharmacology ; Tamoxifen/pharmacology
Chemical Substances	Pyrazoles ; Pyrimidines ; Tamoxifen (094ZI81Y45) ; ibrutinib (1X70OSD4VX)
Language	English
Publishing date	2018-08-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-018-05772-7
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Article ; Online: Atypical chemokine receptor 4 shapes activated B cell fate.

The Journal of experimental medicine

2018 Volume 215, Issue 3, Page(s) 801–813

Abstract: Activated B cells can initially differentiate into three functionally distinct fates-early plasmablasts (PBs), germinal center (GC) B cells, or early memory B cells-by mechanisms that remain poorly understood. Here, we identify atypical chemokine ... ...

Abstract	Activated B cells can initially differentiate into three functionally distinct fates-early plasmablasts (PBs), germinal center (GC) B cells, or early memory B cells-by mechanisms that remain poorly understood. Here, we identify atypical chemokine receptor 4 (ACKR4), a decoy receptor that binds and degrades CCR7 ligands CCL19/CCL21, as a regulator of early activated B cell differentiation. By restricting initial access to splenic interfollicular zones (IFZs), ACKR4 limits the early proliferation of activated B cells, reducing the numbers available for subsequent differentiation. Consequently, ACKR4 deficiency enhanced early PB and GC B cell responses in a CCL19/CCL21-dependent and B cell-intrinsic manner. Conversely, aberrant localization of ACKR4-deficient activated B cells to the IFZ was associated with their preferential commitment to the early PB linage. Our results reveal a regulatory mechanism of B cell trafficking via an atypical chemokine receptor that shapes activated B cell fate.
MeSH term(s)	Animals ; Antigens/metabolism ; B-Lymphocytes/cytology ; B-Lymphocytes/metabolism ; Cell Lineage ; Cell Proliferation ; Germinal Center/metabolism ; Mice, Inbred C57BL ; Receptors, CCR/metabolism ; Spleen/cytology
Chemical Substances	Ackr4 protein, mouse ; Antigens ; Receptors, CCR
Language	English
Publishing date	2018-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20171067
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Ua VI Zs.107: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: FAS Inactivation Releases Unconventional Germinal Center B Cells that Escape Antigen Control and Drive IgE and Autoantibody Production.

Butt, Danyal / Chan, Tyani D / Bourne, Katherine / Hermes, Jana R / Nguyen, Akira / Statham, Aaron / O'Reilly, Lorraine A / Strasser, Andreas / Price, Susan / Schofield, Peter / Christ, Daniel / Basten, Antony / Ma, Cindy S / Tangye, Stuart G / Phan, Tri Giang / Rao, V Koneti / Brink, Robert

Immunity

2015 Volume 42, Issue 5, Page(s) 890–902

Abstract: The mechanistic links between genetic variation and autoantibody production in autoimmune disease remain obscure. Autoimmune lymphoproliferative syndrome (ALPS) is caused by inactivating mutations in FAS or FASL, with autoantibodies thought to arise ... ...

Abstract	The mechanistic links between genetic variation and autoantibody production in autoimmune disease remain obscure. Autoimmune lymphoproliferative syndrome (ALPS) is caused by inactivating mutations in FAS or FASL, with autoantibodies thought to arise through failure of FAS-mediated removal of self-reactive germinal center (GC) B cells. Here we show that FAS is in fact not required for this process. Instead, FAS inactivation led to accumulation of a population of unconventional GC B cells that underwent somatic hypermutation, survived despite losing antigen reactivity, and differentiated into a large population of plasma cells that included autoantibody-secreting clones. IgE(+) plasma cell numbers, in particular, increased after FAS inactivation and a major cohort of ALPS-affected patients were found to have hyper-IgE. We propose that these previously unidentified cells, designated "rogue GC B cells," are a major driver of autoantibody production and provide a mechanistic explanation for the linked production of IgE and autoantibodies in autoimmune disease.
MeSH term(s)	Animals ; Autoantibodies/biosynthesis ; Autoantibodies/immunology ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Fluorescent Antibody Technique ; Germinal Center/cytology ; Germinal Center/immunology ; Humans ; Immunoglobulin E/biosynthesis ; Immunoglobulin E/immunology ; Mice ; Polymerase Chain Reaction ; fas Receptor/deficiency ; fas Receptor/immunology ; fas Receptor/metabolism
Chemical Substances	Autoantibodies ; fas Receptor ; Immunoglobulin E (37341-29-0)
Language	English
Publishing date	2015-05-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2015.04.010
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: T follicular helper cells have distinct modes of migration and molecular signatures in naive and memory immune responses.

Suan, Dan / Nguyen, Akira / Moran, Imogen / Bourne, Katherine / Hermes, Jana R / Arshi, Mehreen / Hampton, Henry R / Tomura, Michio / Miwa, Yoshihiro / Kelleher, Anthony D / Kaplan, Warren / Deenick, Elissa K / Tangye, Stuart G / Brink, Robert / Chtanova, Tatyana / Phan, Tri Giang

Immunity

2015 Volume 42, Issue 4, Page(s) 704–718

Abstract: B helper follicular T (Tfh) cells are critical for long-term humoral immunity. However, it remains unclear how these cells are recruited and contribute to secondary immune responses. Here we show that primary Tfh cells segregate into follicular mantle ( ... ...

Abstract	B helper follicular T (Tfh) cells are critical for long-term humoral immunity. However, it remains unclear how these cells are recruited and contribute to secondary immune responses. Here we show that primary Tfh cells segregate into follicular mantle (FM) and germinal center (GC) subpopulations that display distinct gene expression signatures. Restriction of the primary Tfh cell subpopulation in the GC was mediated by downregulation of chemotactic receptor EBI2. Following collapse of the GC, memory T cells persisted in the outer follicle where they scanned CD169(+) subcapsular sinus macrophages. Reactivation and intrafollicular expansion of these follicular memory T cells in the subcapsular region was followed by their extrafollicular dissemination via the lymphatic flow. These data suggest that Tfh cells integrate their antigen-experience history to focus T cell help within the GC during primary responses but act rapidly to provide systemic T cell help after re-exposure to the antigen.
MeSH term(s)	Animals ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; Cell Differentiation ; Cell Lineage/genetics ; Cell Lineage/immunology ; Cell Movement/immunology ; Cell Proliferation ; Gene Expression Profiling ; Gene Expression Regulation ; Germinal Center/cytology ; Germinal Center/immunology ; Immunity, Humoral ; Immunologic Memory ; Mice ; Mice, Knockout ; Primary Cell Culture ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/immunology ; Sialic Acid Binding Ig-like Lectin 1/genetics ; Sialic Acid Binding Ig-like Lectin 1/immunology ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology ; T-Lymphocytes, Helper-Inducer/immunology
Chemical Substances	Gpr183 protein, mouse ; Receptors, G-Protein-Coupled ; Sialic Acid Binding Ig-like Lectin 1 ; Siglec1 protein, mouse
Language	English
Publishing date	2015-04-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2015.03.002
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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