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Article ; Online: Interleukin-4 downregulates transcription factor BCL6 to promote memory B cell selection in germinal centers.

Shehata, Laila / Thouvenel, Christopher D / Hondowicz, Brian D / Pew, Lucia A / Pritchard, Gretchen Harms / Rawlings, David J / Choi, Jinyong / Pepper, Marion

Immunity

2024 Volume 57, Issue 4, Page(s) 843–858.e5

Abstract: Germinal center (GC)-derived memory B cells (MBCs) are critical for humoral immunity as they differentiate into protective antibody-secreting cells during re-infection. GC formation and cellular interactions within the GC have been studied in detail, yet ...

Abstract	Germinal center (GC)-derived memory B cells (MBCs) are critical for humoral immunity as they differentiate into protective antibody-secreting cells during re-infection. GC formation and cellular interactions within the GC have been studied in detail, yet the exact signals that allow for the selection and exit of MBCs are not understood. Here, we showed that IL-4 cytokine signaling in GC B cells directly downregulated the transcription factor BCL6 via negative autoregulation to release cells from the GC program and to promote MBC formation. This selection event required additional survival cues and could therefore result in either GC exit or death. We demonstrate that both increasing IL-4 bioavailability or limiting IL-4 signaling disrupted MBC selection stringency. In this way, IL-4 control of BCL6 expression serves as a tunable switch within the GC to tightly regulate MBC selection and affinity maturation.
MeSH term(s)	B-Lymphocytes ; Germinal Center ; Interleukin-4/metabolism ; Memory B Cells ; Proto-Oncogene Proteins c-bcl-6/genetics ; Proto-Oncogene Proteins c-bcl-6/metabolism ; Transcription Factors/metabolism
Chemical Substances	Interleukin-4 (207137-56-2) ; Proto-Oncogene Proteins c-bcl-6 ; Transcription Factors
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2024.02.018
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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: Allergen exposure functionally alters influenza-specific CD4+ Th1 memory cells in the lung.

Rüterbusch, Mikel J / Hondowicz, Brian D / Takehara, Kennidy K / Pruner, Kurt B / Griffith, Thomas S / Pepper, Marion

The Journal of experimental medicine

2023 Volume 220, Issue 11

Abstract: CD4+ lung-resident memory T cells (TRM) generated in response to influenza infection confer effective protection against subsequent viral exposures. Whether these cells can be altered by environmental antigens and cytokines released during heterologous, ... ...

Abstract	CD4+ lung-resident memory T cells (TRM) generated in response to influenza infection confer effective protection against subsequent viral exposures. Whether these cells can be altered by environmental antigens and cytokines released during heterologous, antigen-independent immune responses is currently unclear. We therefore investigated how influenza-specific CD4+ Th1 TRM in the lung are impacted by a subsequent Th2-inducing respiratory house dust mite (HDM) exposure. Although naïve influenza-specific CD4+ T cells in the lymph nodes do not respond to HDM, influenza-specific CD4+ TRM in the lungs do respond to a subsequent allergen exposure by decreasing expression of the transcription factor T-bet. This functional alteration is associated with decreased IFN-γ production upon restimulation and improved disease outcomes following heterosubtypic influenza challenge. Further investigation revealed that ST2 signaling in CD4+ T cells during allergic challenge is necessary to induce these changes in lung-resident influenza-specific CD4+ TRM. Thus, heterologous antigen exposure or ST2-signaling can drive persistent changes in CD4+ Th1 TRM populations and impact protection upon reinfection.
MeSH term(s)	Animals ; Humans ; Influenza, Human ; Interleukin-1 Receptor-Like 1 Protein ; CD4-Positive T-Lymphocytes ; Th1 Cells ; Pyroglyphidae ; Allergens
Chemical Substances	Interleukin-1 Receptor-Like 1 Protein ; Allergens
Language	English
Publishing date	2023-09-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20230112
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Article: IL-4 downregulates BCL6 to promote memory B cell selection in germinal centers.

Shehata, Laila / Thouvenel, Christopher D / Hondowicz, Brian D / Pew, Lucia A / Rawlings, David J / Choi, Jinyong / Pepper, Marion

bioRxiv : the preprint server for biology

2023

Abstract	Germinal center (GC)-derived memory B cells (MBCs) are critical for humoral immunity as they differentiate into protective antibody-secreting cells during re-infection. GC formation and cellular interactions within the GC have been studied in detail, yet the exact signals that allow for the selection and exit of MBCs are not understood. Here, we show that IL-4 signaling in GC B cells directly downregulates BCL6 via negative autoregulation to release cells from the GC program and promote MBC formation. This selection event requires additional survival cues and can therefore result in either GC exit or death. We demonstrate that both increasing IL-4 bioavailability or limiting IL-4 signaling disrupt MBC selection stringency. In this way, IL-4 control of BCL6 expression serves as a tunable switch within the GC to tightly regulate MBC selection and affinity maturation.
Language	English
Publishing date	2023-10-04
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.26.525749
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Article ; Online: IL-2 is required for the generation of viral-specific CD4

Hondowicz, Brian D / Kim, Karen S / Ruterbusch, Mikel J / Keitany, Gladys J / Pepper, Marion

European journal of immunology

2017 Volume 48, Issue 1, Page(s) 80–86

Abstract: ... ...

Abstract	CD4
MeSH term(s)	Animals ; Antigens, Viral/immunology ; B-Lymphocytes/immunology ; Female ; Immunologic Memory/genetics ; Immunologic Memory/immunology ; Interleukin-2/genetics ; Interleukin-2/immunology ; Lung/cytology ; Lung/immunology ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic Choriomeningitis/pathology ; Lymphocytic Choriomeningitis/virology ; Lymphocytic choriomeningitis virus/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Th1 Cells/immunology ; Th2 Cells/immunology
Chemical Substances	Antigens, Viral ; Interleukin-2
Language	English
Publishing date	2017-10-13
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201746928
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Zs.A 489: 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: Blood Stage Malaria Disrupts Humoral Immunity to the Pre-erythrocytic Stage Circumsporozoite Protein.

Keitany, Gladys J / Kim, Karen S / Krishnamurty, Akshay T / Hondowicz, Brian D / Hahn, William O / Dambrauskas, Nicholas / Sather, D Noah / Vaughan, Ashley M / Kappe, Stefan H I / Pepper, Marion

Cell reports

2016 Volume 17, Issue 12, Page(s) 3193–3205

Abstract: Many current malaria vaccines target the pre-erythrocytic stage of infection in the liver. However, in malaria-endemic regions, increased blood stage exposure is associated with decreased vaccine efficacy, thereby challenging current vaccine efforts. We ... ...

Abstract	Many current malaria vaccines target the pre-erythrocytic stage of infection in the liver. However, in malaria-endemic regions, increased blood stage exposure is associated with decreased vaccine efficacy, thereby challenging current vaccine efforts. We hypothesized that pre-erythrocytic humoral immunity is directly disrupted by blood stage infection. To investigate this possibility, we used Plasmodium-antigen tetramers to analyze B cells after infection with either late liver stage arresting parasites or wild-type parasites that progress to the blood stage. Our data demonstrate that immunoglobulin G (IgG) antibodies against the pre-erythrocytic antigen, circumsporozoite protein (CSP), are generated only in response to the attenuated, but not the wild-type, infection. Further analyses revealed that blood stage malaria inhibits CSP-specific germinal center B cell differentiation and modulates chemokine expression. This results in aberrant memory formation and the loss of a rapid secondary B cell response. These data highlight how immunization with attenuated parasites may drive optimal immunity to malaria.
MeSH term(s)	Animals ; Antigens, Protozoan/immunology ; B-Lymphocytes/immunology ; B-Lymphocytes/parasitology ; Erythrocytes/immunology ; Erythrocytes/parasitology ; Humans ; Immunity, Humoral ; Immunoglobulin G/immunology ; Liver/immunology ; Liver/parasitology ; Malaria Vaccines/immunology ; Malaria Vaccines/therapeutic use ; Malaria, Falciparum/genetics ; Malaria, Falciparum/immunology ; Malaria, Falciparum/parasitology ; Plasmodium falciparum/immunology ; Plasmodium falciparum/pathogenicity ; Vaccination
Chemical Substances	Antigens, Protozoan ; Immunoglobulin G ; Malaria Vaccines
Language	English
Publishing date	2016-12-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2016.11.060
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Article: T cell-mediated activation and regulation of anti-chromatin B cells.

Pagán, Antonio J / Ramón, Hilda E / Hondowicz, Brian D / Erikson, Jan

Autoimmunity reviews

2006 Volume 5, Issue 6, Page(s) 373–376

Abstract: We have taken an immunoglobulin transgenic approach to study how self-reactive B cells are held in check in healthy mice and what parameters contribute to their activation in autoimmunity. Using this strategy, we have documented that a population of anti- ...

Abstract	We have taken an immunoglobulin transgenic approach to study how self-reactive B cells are held in check in healthy mice and what parameters contribute to their activation in autoimmunity. Using this strategy, we have documented that a population of anti-chromatin B cells migrate to the periphery. In a healthy background, these cells have a reduced lifespan, appear developmentally arrested, and localize primarily to the T/B cell interface in the spleen. Importantly, they are capable of differentiating into antibody-forming cells when provided with T cell help. T(H)1 and T(H)2 cells induce IgG2a and IgG1 autoantibodies, respectively. In the context of the autoimmune-prone lpr/lpr or gld/gld mutations, these autoreactive B cells populate the B cell follicle, and this is dependent upon CD4 T cells. However, after 10 weeks of age serum autoantibodies are produced. We hypothesize that control of autoantibody production in young autoimmune-prone mice is regulated by the counterbalancing influence of regulatory T cells. We show that while autoantibody production is blocked in the context of regulatory T cells, early events characterizing a productive T cell-B cell interaction are not disturbed, with the notable exceptions of T(H) ICOS levels and IFN-gamma and IL-10 production.
MeSH term(s)	Animals ; Antibody Formation ; Autoantibodies/physiology ; B-Lymphocytes/immunology ; B-Lymphocytes/physiology ; Chromatin/immunology ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Models, Immunological ; T-Lymphocytes/physiology
Chemical Substances	Autoantibodies ; Chromatin
Language	English
Publishing date	2006-07
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2144145-5
ISSN	1568-9972
ISSN	1568-9972
DOI	10.1016/j.autrev.2005.10.011
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Zs.A 5913: Show issues

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Article ; Online: ICOS expression by effector T cells influences the ability of regulatory T cells to inhibit anti-chromatin B cell responses in recipient mice.

Hondowicz, Brian D / Batheja, Amrita O / Metzgar, Michele H / Caton, Andrew J / Erikson, Jan

Journal of autoimmunity

2009 Volume 34, Issue 4, Page(s) 460–468

Abstract: T regulatory cells are critical for the prevention of autoimmunity. Specifically, Treg cells can control anti-chromatin antibody production in vivo, and this correlates with decreased ICOS expression on CD4(+) T helper cells. Here we test the ... ...

Abstract	T regulatory cells are critical for the prevention of autoimmunity. Specifically, Treg cells can control anti-chromatin antibody production in vivo, and this correlates with decreased ICOS expression on CD4(+) T helper cells. Here we test the significance of high ICOS expression by T effector cells, firstly in terms of the anti-chromatin B cell response, and secondly on the ability of Treg cells to suppress T cell help. We bred CD4(+) T cell receptor transgenic mice with mice that carry the Roquin(san/san) mutation. The Roquin gene functions to limit ICOS mRNA such that CD4 T cells from mutant mice express elevated ICOS. Using an in vivo model, TS1.Roquin(san/san) Th cells were compared with wild-type TS1 Th cells with regard to their ability to help anti-chromatin B cells in the presence or absence of Treg cells. Both TS1 and TS1.Roquin(san/san) Th cells induced anti-chromatin IgM(a) antibodies, but the TS1.Roquin(san/san) Th cells resulted in the recovery of more class-switched and germinal center B cells. Neither source of Th cells were capable of inducing long-lived autoantibodies. Treg cells completely suppressed anti-chromatin IgM(a) antibody production and reduced anti-chromatin B cell recovery induced by TS1 Th cells. Importantly, this suppression was less effective when TS1.Roquin(san/san) Th cells were used. Thus, high ICOS levels on effector T cells results in autoimmunity by augmenting the autoreactive B cell response and by dampening the effect of Treg cell suppression.
MeSH term(s)	Animals ; Antigens, Differentiation, T-Lymphocyte/biosynthesis ; Antigens, Differentiation, T-Lymphocyte/physiology ; Autoantibodies/biosynthesis ; Autoimmunity ; B-Lymphocytes/immunology ; Cell Communication/immunology ; Chromatin/immunology ; Inducible T-Cell Co-Stimulator Protein ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes, Helper-Inducer/metabolism ; T-Lymphocytes, Regulatory/immunology ; Ubiquitin-Protein Ligases/genetics
Chemical Substances	Antigens, Differentiation, T-Lymphocyte ; Autoantibodies ; Chromatin ; Icos protein, mouse ; Inducible T-Cell Co-Stimulator Protein ; Rc3h1 protein, mouse (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2009-12-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2009.11.016
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Article ; Online: Interleukin-2-Dependent Allergen-Specific Tissue-Resident Memory Cells Drive Asthma.

Hondowicz, Brian D / An, Dowon / Schenkel, Jason M / Kim, Karen S / Steach, Holly R / Krishnamurty, Akshay T / Keitany, Gladys J / Garza, Esteban N / Fraser, Kathryn A / Moon, James J / Altemeier, William A / Masopust, David / Pepper, Marion

Immunity

2015 Volume 44, Issue 1, Page(s) 155–166

Abstract: Exposure to inhaled allergens generates T helper 2 (Th2) CD4(+) T cells that contribute to episodes of inflammation associated with asthma. Little is known about allergen-specific Th2 memory cells and their contribution to airway inflammation. We ... ...

Abstract	Exposure to inhaled allergens generates T helper 2 (Th2) CD4(+) T cells that contribute to episodes of inflammation associated with asthma. Little is known about allergen-specific Th2 memory cells and their contribution to airway inflammation. We generated reagents to understand how endogenous CD4(+) T cells specific for a house dust mite (HDM) allergen form and function. After allergen exposure, HDM-specific memory cells persisted as central memory cells in the lymphoid organs and tissue-resident memory cells in the lung. Experimental blockade of lymphocyte migration demonstrated that lung-resident cells were sufficient to induce airway hyper-responsiveness, which depended upon CD4(+) T cells. Investigation into the differentiation of pathogenic Trm cells revealed that interleukin-2 (IL-2) signaling was required for residency and directed a program of tissue homing migrational cues. These studies thus identify IL-2-dependent resident Th2 memory cells as drivers of lung allergic responses.
MeSH term(s)	Allergens/immunology ; Animals ; Antigens, Dermatophagoides/immunology ; Asthma/immunology ; Cell Differentiation/immunology ; Cell Separation ; Disease Models, Animal ; Female ; Immunologic Memory/immunology ; Interleukin-2/immunology ; Lung/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Pyroglyphidae/immunology ; Th2 Cells/immunology
Chemical Substances	Allergens ; Antigens, Dermatophagoides ; Interleukin-2
Language	English
Publishing date	2015-12-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2015.11.004
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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: Autoantibody production in lpr/lpr gld/gld mice reflects accumulation of CD4+ effector cells that are resistant to regulatory T cell activity.

Hondowicz, Brian D / Fields, Michele L / Nish, Simone A / Larkin, Joseph / Caton, Andrew J / Erikson, Jan

Journal of autoimmunity

2008 Volume 31, Issue 2, Page(s) 98–109

Abstract: In Fas/FasL-deficient mice anti-chromatin Ab production is T cell dependent and is not apparent until after 10 weeks of age. Early control of anti-chromatin antibodies may be due to the counterbalancing influence of Treg cells. Here we show that Treg ... ...

Abstract	In Fas/FasL-deficient mice anti-chromatin Ab production is T cell dependent and is not apparent until after 10 weeks of age. Early control of anti-chromatin antibodies may be due to the counterbalancing influence of Treg cells. Here we show that Treg cells block lpr/lpr gld/gld Th cells from providing help to anti-chromatin B cells in an in vivo transfer system. Interestingly, the percentage and absolute numbers of Foxp3+ Treg cells is elevated in BALB/c-lpr/lpr gld/gld mice and increases with age compared to BALB/c mice. The majority of Foxp3 expression is found in the B220- CD4+ T cell population, and Foxp3-expressing cells are localized in the splenic PALS (periarteriolar lymphocyte sheath). Strikingly, although the lack of functional Fas/FasL does not affect the ability of Treg cells to block Th cell proliferation, Treg cells can block the IFN-gamma differentiation of Th cells from BALB/c or young BALB-lpr/lpr gld/gld mice but not of pre-existing Th1 cells from older BALB/c-lpr/lpr gld/gld mice. Thus, we suggest autoantibody production is not caused by the lack of Treg cells but by a defect in activation-induced cell death that leads to the accumulation of T effector cells that are resistant to regulatory T cell activity.
MeSH term(s)	Adoptive Transfer ; Animals ; Autoantibodies/biosynthesis ; B-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/immunology ; Female ; Forkhead Transcription Factors/metabolism ; Interferon-gamma/metabolism ; Interleukin-4/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred MRL lpr ; Mice, Mutant Strains ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Autoantibodies ; FOXP3 protein, human ; Forkhead Transcription Factors ; Interleukin-4 (207137-56-2) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2008-06-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639452-8
ISSN	0896-8411
ISSN	0896-8411
DOI	10.1016/j.jaut.2008.04.022
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Article ; Online: Efficient help for autoreactive B-cell activation requires CD4+ T-cell recognition of an agonist peptide at the effector stage.

Hondowicz, Brian D / Batheja, Amrita O / Metzgar, Michele H / Pagán, Antonio J / Perng, Olivia A / Willms, Simone / Caton, Andrew J / Erikson, Jan

European journal of immunology

2009 Volume 39, Issue 9, Page(s) 2377–2382

Abstract: T-cell recognition of peptide/MHC complexes is flexible and can lead to differential activation, but how interactions with agonist (full activation) or partial agonist (suboptimal activation) peptides can shape immune responses in vivo is not well ... ...

Abstract	T-cell recognition of peptide/MHC complexes is flexible and can lead to differential activation, but how interactions with agonist (full activation) or partial agonist (suboptimal activation) peptides can shape immune responses in vivo is not well characterized. We investigated the effect of stimulation by agonist or partial agonist ligands during initial CD4(+) T-cell priming, and subsequent T-B-cell cognate interactions, on antibody production by anti-chromatin B cells. We found that autoantibody production required TCR recognition of an agonist peptide at the effector stage of B-cell activation. However, interaction with a weak agonist ligand at this effector stage failed to promote efficient autoantibody production, even if the CD4(+) T cells were fully primed by an agonist peptide. These studies suggest that the reactivity of the TCR for a target self-peptide during CD4(+) T-B-cell interaction can be a critical determinant in restraining anti-chromatin autoantibody production.
MeSH term(s)	Animals ; Autoantibodies/immunology ; Autoantibodies/metabolism ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; CD4-Positive T-Lymphocytes/immunology ; Chromatin/immunology ; Female ; Histocompatibility Antigens Class II/immunology ; Immunoglobulin Class Switching ; Lymphocyte Activation/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Peptides/immunology ; Receptors, Antigen, T-Cell/immunology ; Receptors, Antigen, T-Cell/metabolism ; Th1 Cells/immunology ; Th1 Cells/metabolism
Chemical Substances	Autoantibodies ; Chromatin ; Histocompatibility Antigens Class II ; Peptides ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2009-08-07
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.200939471
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