B1 Cells | ScienceGate

ABSTRACT Studies utilizing various immunodeficient mouse models of rotavirus (RV) infection demonstrated significant roles of RV-specific secretory immunoglobulin A (IgA), CD4+ T cells, and CD8+T cells in the clearance of RV and protection from secondary infection. Secretion of small but detectable amounts of IgA in RV-infected αβ T-cell receptor knockout mice (11) and distinctive anatomical localization and physiology of B1 cells suggested that B1 cells might be capable of producing RV-specific intestinal IgA in a T-cell-independent fashion and, therefore, be responsible for ablation of RV shedding. We investigated the role of B1 cells in the resolution of primary RV infection using a SCID mouse model. We found that the adoptive transfer of unseparated peritoneal exudate cells ablates RV shedding and leads to the production of high levels of RV-specific intestinal IgA. In contrast, purified B1 cells do not ablate RV shedding and do not induce a T-cell-independent or T-cell-dependent, RV-specific IgA response but do secrete large amounts of polyclonal (total) intestinal IgA. Cotransfer of mixtures of purified B1 cells and B1-cell-depleted peritoneal exudate cells differing in IgA allotypic markers also demonstrated that B2 cells (B1-cell-depleted peritoneal exudate cells) and not B1 cells produced RV-specific IgA. To our knowledge, this is the first observation that B1 cells are unable to cooperate with CD4+ T cells and produce virus-specific intestinal IgA antibody. We also observed that transferred CD4+ T cells alone are capable of resolving RV shedding, although no IgA is secreted. These data suggest that RV-specific IgA may not be obligatory for RV clearance but may protect from reinfection and that effector CD4+ T cells alone can mediate the resolution of primary RV infection. Reconstitution of RV-infected SCID mice with B1 cells results in the outgrowth of contaminating, donor CD4+ T cells that are unable to clear RV, possibly because their oligoclonal specificities may be ineffective against RV antigens.

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Human B1 cells in umbilical cord and adult peripheral blood express the novel phenotype CD20+CD27+CD43+CD70−

Journal of Experimental Medicine ◽

10.1084/jem.201014992084c ◽

2011 ◽

Vol 208 (4) ◽

pp. 871-871 ◽

Cited By ~ 3

Author(s):

Daniel O. Griffin ◽

Nichol E. Holodick ◽

Thomas L. Rothstein

Keyword(s):

Umbilical Cord ◽

Peripheral Blood ◽

The Novel ◽

B1 Cells ◽

Adult Peripheral Blood

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B-1 cell: the precursor of a novel mononuclear phagocyte with immuno-regulatory properties

Anais da Academia Brasileira de Ciências ◽

10.1590/s0001-37652009000300013 ◽

2009 ◽

Vol 81 (3) ◽

pp. 489-496 ◽

Cited By ~ 11

Author(s):

José Daniel Lopes ◽

Mario Mariano

Keyword(s):

Mammalian Cells ◽

Giant Cells ◽

Mononuclear Phagocyte ◽

Different Types ◽

Series Of Experiments ◽

B1 Cells ◽

Regulatory Properties

Characterization of the origin, properties, functions and fate of cells is a fundamental task for the understanding of physiological and pathological phenomena. Despite the bulk of knowledge concerning the diverse characteristics of mammalian cells, some of them, such as B-1 cells, are still poorly understood. Here we report the results obtained in our laboratory on these cells in the last 10 years. After showing that B-1 cells could be cultured and amplified in vitro, a series of experiments were performed with these cells. They showed that B1 cells reside mostly in the peritoneal and pleural cavities, migrate to distant inflammatory foci, coalesce to form giant cells and participate in granuloma formation, both in vitro and in vivo. They are also able to present antigens to immunologically responsive cells and are endowed with regulatory properties. Further, we have also shown that these cells facilitate different types of infection as well as tumor growth and spreading. These data are presently reviewed pointing to a pivotal role that these cells may play in innate and acquired immunity.

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002 Tumor-infiltrating CD5+ regulatory B1 cells suppress melanoma tumor immunity via inhibiting cytokine production of tumor-infiltrating CD8+ T cells

Journal of Investigative Dermatology ◽

10.1016/j.jid.2018.03.006 ◽

2018 ◽

Vol 138 (5) ◽

pp. S1

Author(s):

T. Kobayashi ◽

T. Matsushita ◽

Y. Hamaguchi ◽

M. Fujimoto ◽

K. Takehara

Keyword(s):

T Cells ◽

Tumor Immunity ◽

Cd8 T Cells ◽

Cytokine Production ◽

Melanoma Tumor ◽

B1 Cells

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ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions

BMC Immunology ◽

10.1186/s12865-019-0330-z ◽

2019 ◽

Vol 20 (1) ◽

Author(s):

Polyxeni T. Mantani ◽

Pontus Dunér ◽

Irena Ljungcrantz ◽

Jan Nilsson ◽

Harry Björkbacka ◽

...

Keyword(s):

Apolipoprotein E ◽

Lipid Content ◽

Cell Expansion ◽

Killer Cell ◽

Flow Cytometric Analysis ◽

Lymphoid Cells ◽

Direct Role ◽

Atherosclerotic Lesions ◽

B1 Cells

Abstract Background Expansion of type 2 innate lymphoid cells (ILC2s) in hypercholesterolaemic mice protects against atherosclerosis while different ILC2 subsets have been described (natural, inflammatory) based on their suppression of tumorigenicity 2 (ST2) and killer-cell lectin like receptor G1 (KLRG1) expression. The aim of the current study is to characterize the interleukin 25 (IL25)-induced splenic ILC2 population (Lin−CD45+IL17RB+ICOS+IL7raintermediate) and address its direct role in experimental atherosclerosis by its adoptive transfer to hypercholesterolaemic apolipoprotein E deficient (apoE−/−) mice. Results Immunomagnetically enriched, FACS-sorted ILC2s from the spleens of IL-25 treated apoE−/− mice were stained for KLRG1 and ST2 directly upon cell obtainment or in vitro cell expansion for flow cytometric analysis. IL25-induced splenic ILC2s express high levels of both KLRG1 and ST2. However, both markers are downregulated upon in vitro cell expansion. In vitro expanded splenic ILC2s were intraperitoneally transferred to apoE−/− recipients on high fat diet. ApoE−/− mice that received in vitro expanded splenic ILC2s had decreased lipid content in subvalvular heart and brachiocephalic artery (BCA) plaques accompanied by increased peritoneal B1 cells, activated eosinophils and alternatively activated macrophages (AAMs) as well as anti-phosphorylcholine (PC) immunoglobulin (Ig) M in plasma. Conclusions With the current data we designate the IL25-induced ILC2 population to decrease the lipid content of atherosclerotic lesions in apoE−/− mice and we directly link the induction of B1 cells and the atheroprotective anti-PC IgM antibodies with ILC2s.

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New insights into immune mechanisms of antiperlecan/LG3 antibody production: Importance of T cells and innate B1 cells

American Journal of Transplantation ◽

10.1111/ajt.15082 ◽

2018 ◽

Vol 19 (3) ◽

pp. 699-712 ◽

Cited By ~ 7

Author(s):

Lauriane Padet ◽

Mélanie Dieudé ◽

Annie Karakeussian‐Rimbaud ◽

Bing Yang ◽

Julie Turgeon ◽

...

Keyword(s):

T Cells ◽

Antibody Production ◽

Immune Mechanisms ◽

B1 Cells

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Overexpression of the CXCR5 chemokine receptor, and its ligand, CXCL13 in B-cell chronic lymphocytic leukemia

Blood ◽

10.1182/blood-2007-05-089409 ◽

2007 ◽

Vol 110 (9) ◽

pp. 3316-3325 ◽

Cited By ~ 130

Author(s):

Andrea Bürkle ◽

Matthias Niedermeier ◽

Annette Schmitt-Gräff ◽

William G. Wierda ◽

Michael J. Keating ◽

...

Keyword(s):

B Cells ◽

Chronic Lymphocytic Leukemia ◽

B Cell ◽

Actin Polymerization ◽

Serum Levels ◽

Lymphocytic Leukemia ◽

Lymphoid Tissues ◽

Accessory Cells ◽

Mitogen Activated Protein ◽

B1 Cells

Abstract CXCL13 is a homeostatic chemokine for lymphocyte homing and positioning within follicles of secondary lymphoid tissues, acting through its cognate receptor, CXCR5. Moreover, the CXCR5-CXCL13 axis plays a unique role in trafficking and homing of B1 cells. Here, we report that chronic lymphocytic leukemia (CLL) B cells express high levels of functional CXCR5. CXCR5 expression levels were similar on CLL B cells and normal CD5+ B cells, and higher compared with normal CD5− B cells, follicular B-helper T cells (TFH cells), or neoplastic B cells from other B-cell neoplasias. Stimulation of CLL cells with CXCL13 induces actin polymerization, CXCR5 endocytosis, chemotaxis, and prolonged activation of p44/42 mitogen-activated protein kinases. Anti-CXCR5 antibodies, pertussis toxin, and wortmannin inhibited chemotaxis to CXCL13, demonstrating the importance of Gi proteins and PI3 kinases for CXCR5 signaling. Moreover, CLL patients had significantly higher CXCL13 serum levels than volunteers, and CXCL13 levels correlated with β2 microglobulin. We detected CXCL13 mRNA expression by nurselike cells, and high levels of CXCL13 protein in supernatants of CLL nurselike cell cultures. By immunohistochemistry, we detected CXCL13+ expression by CD68+ macrophages in situ within CLL lymph nodes. These data suggest that CXCR5 plays a role in CLL cell positioning and cognate interactions between CLL and CXCL13-secreting CD68+ accessory cells in lymphoid tissues.

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