DNA Microarray Gene Expression Profile of Marginal Zone versus Follicular B Cells and Idiotype Positive Marginal Zone B Cells before and after Immunization with <i>Streptococcus pneumoniae</i>

Kin, Nicholas W.; Crawford, Dianna M.; Liu, Jiabin; Behrens, Timothy W.; Kearney, John F.

doi:10.4049/jimmunol.180.10.6663

Cited by 49 publications

(49 citation statements)

References 45 publications

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“…We observed a progressive increase in expression as B cells mature in the bone marrow. In the spleen, we found Klf3 levels to be lowest in MZ cells, in agreement with previous data comparing gene expression in purified FO and MZ B cell populations (56). This might imply that low levels of Klf3 promote MZ cell development.…”

Section: Klf3 Is Differentially Expressed During B Cell Development Asupporting

confidence: 80%

Impaired B Cell Development in the Absence of Krüppel-like Factor 3

Vũ

Gatto

Turner

et al. 2011

The Journal of Immunology

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Krüppel-like factor 3 (Klf3) is a member of the Klf family of transcription factors. Klfs are widely expressed and have diverse roles in development and differentiation. In this study, we examine the function of Klf3 in B cell development by studying B lymphopoiesis in a Klf3 knockout mouse model. We show that B cell differentiation is significantly impaired in the bone marrow, spleen, and peritoneal cavity of Klf3 null mice and confirm that the defects are cell autonomous. In the bone marrow, there is a reduction in immature B cells, whereas recirculating mature cells are noticeably increased. Immunohistology of the spleen reveals a poorly structured marginal zone (MZ) that may in part be caused by deregulation of adhesion molecules on MZ B cells. In the peritoneal cavity, there are significant defects in B1 B cell development. We also report that the loss of Klf3 in MZ B cells is associated with reduced BCR signaling strength and an impaired ability to respond to LPS stimulation. Finally, we show increased expression of a number of Klf genes in Klf3 null B cells, suggesting that a Klf regulatory network may exist in B cells.

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Section: Klf3 Is Differentially Expressed During B Cell Development Asupporting

confidence: 80%

Impaired B Cell Development in the Absence of Krüppel-like Factor 3

Vũ

Gatto

Turner

et al. 2011

The Journal of Immunology

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“…The resulting set of 2737 genes associated with MZ B cells versus follicular B cells included most of those previously identified in a similar comparison. 33 As shown in supplemental Figure 2B, using these 2737 genes to determine the relatedness of follicular and MZ B-cell subsets from normal and transgenic mice, we found that transgenic MZ B cells, and, surprisingly, transgenic follicular B cells, clustered together with normal MZ B cells. This was unlike in a purely computed (unsupervised) clustering where follicular and MZ B cells were grouped together irrespective of being transgenic or not (supplemental Figure 2A).…”

Section: Klf3 Induces a Mz B-cell Signature Within Follicular B Cellsmentioning

confidence: 99%

Programming of marginal zone B-cell fate by basic Krüppel-like factor (BKLF/KLF3)

Turchinovich

Vũ

Frommer

et al. 2011

Blood

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IntroductionSp/Krüppel-like factors (KLFs) encompass more than 20 transcription factors in mice or humans. All KLFs share a characteristic DNA-binding domain at their C-terminus consisting of 3 Krüppel-like zinc-finger domains. One subset of KLFs, containing the PXDLS/T motive, recruits the C-terminal binding protein 2 general transcriptional repressor (CtBP2). 1 Apart from this motive, no consensus sequences are found in the N-terminal domain of KLFs. For KLF3 an interaction with four and a half LIM domains 3 protein (FHL3) has been demonstrated. 2 KLFs are involved in differentiation, proliferation, or trafficking of cells in various tissues. 3 They are differentially expressed in lymphocytes, including T cells. Here, KLF2 and few other KLFs have been studied extensively. [4][5][6][7][8] To date, little is known about the role of KLFs in B-cell development.Before colonizing secondary lymphoid organs, such as spleen or lymph nodes, B cells differentiate from hematopoietic precursors in the bone marrow. After the developmental processes there, most of the immature/transitional B cells that are IgM hi CD24 hi IgD lo CD93 hi (AA4.1, 493) CD21/35 Ϫ CD23 Ϫ migrate via the blood to the spleen where they complete their maturation. During splenic maturation, they down-modulate CD93, gain CD21/35 and CD23 expression, and, finally, appear as mature follicular or marginal zone (MZ) B cells, together referred to as B2 cells. Mature follicular and MZ B cells differentially express several cell surface markers: follicular B cells are CD21/35 ϩ CD23 ϩ CD1d lo , whereas MZ B cells are CD21/35 hi CD23 Ϫ CD1d hi ; both express IgM and IgD, but to different levels (IgM lo IgD hi and IgM hi IgD lo for follicular and MZ B cells, respectively). 9 Another lineage of B cells, the B1 subset, localizes predominantly to the peritoneum. These derive mostly from fetal hematopoietic stem cells, as opposed to adult bone marrow stem cells, and require the spleen for maturation. In the spleen, follicular and MZ B cells are localized differently: naive follicular B cells constitute the white pulp follicles that enwrap the T cell-rich periarteriolar zone, surrounding the central ateriole. Branching off the central ateriole, small vessels end openly into the marginal sinus at the white pulp and red pulp interface. This zone is termed "marginal zone" and contains resident macrophages, dendritic cells, and MZ B cells. Here, blood-borne pathogens and microbial products come by contact with the immune systems' tissue first. Thought of as a first line of defense, MZ B cells can initiate rapid T cellindependent antibody responses. 10 Thus, the function of MZ B cells is dependent on their proper localization.Whereas integrins mediate their adhesion, 11,12 chemoattractant molecules define where MZ B cells home to. They are attracted by sphingosine-1-phospate (S1P), with the highest concentration *F.F., J.K., and S.S. contributed equally to this study.The online version of this article contains a data supplement.The publication costs of this article were ...

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“…In addition, haemopoietic stem and progenitor cells, megakaryocytes and mast cells display medium levels of expression. Additional recent micro-array-based studies have also indicated that, within the population of splenic B cells, there is preferential expression of D6 in marginal zone B cells compared with follicular B cells [77]. It is not easy to implicate these cells, especially B cells and HSC in chemokine scavenging at inflamed sites and so we are currently attempting to define alternative roles for D6 on these cell types.…”

Section: D6 Expression By Leukocytesmentioning

confidence: 99%

D6 and the atypical chemokine receptor family: Novel regulators of immune and inflammatory processes

2009

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Chemokines are key regulators of leukocyte migration and play important roles in a number of physiological and pathological immune and inflammatory contexts. In addition to the classical signalling chemokine receptors there has emerged, recently, a new subclass of atypical chemokine receptors. This subfamily is characterised by an apparent lack of signalling and, in some cases, by an ability to internalise and degrade chemokine ligands. This review describes the family of atypical chemokine receptors with particular emphasis on the D6 receptor. The in vitro and in vivo biology of D6 is described, which indicates that D6 is active as a scavenger of inflammatory CC-chemokines and appears to play essential roles in the regulation of inflammatory responses.Key words: Chemokines . Immune regulation . Inflammation IntroductionThe movement of leukocytes during immune and inflammatory responses is a carefully orchestrated process that ensures coordinated cellular migration in response to physiological and pathological cues. Prominent amongst the regulators of leukocyte movement are the members of the chemokine family [1]. Chemokines are small proteins (8-12 kDa) and membership of the chemokine family is defined on the basis of the presence of variations on a conserved cysteine motif in the mature section of the proteins. Chemokines can be assigned to one of four subfamilies according to the specific nature of this motif. The majority of chemokines have four cysteines with 28 chemokines being assigned to the CC family (so-called because of the juxtaposition of the first two cysteine residues) and 16 being assigned to the CXC family (which possess a single variable amino acid between the first two cysteines). The two smaller subfamilies are represented by single members and are the CX3C family (three amino acids between the first two cyteines) and the XC family, which lacks the first and third cyteines seen in the other family members. Much confusion arose in the mid-1990s due to the complex and variable nomenclature used to refer to chemokines. For this reason a systematic nomenclature system has been adopted, which refers to the chemokines as ligands of each of the subfamilies and numbers them according to when their sequences were first deposited in the Genbank databases [2]. Thus, CCL1 is the first CC chemokine to be identified and CCL28 the most recent. Chemokines and their roles in leukocyte migrationFunctionally, chemokines are known to be pleiotropic. However, their main role is in the regulation of leukocyte migration. In this context we can define chemokines as being either homeostatic/ constitutive or inflammatory according to the contexts in which they function [2,3]. Homeostatic chemokinesThe homeostatic chemokines are important for the regulation of basal leukocyte trafficking and regulate processes such as the Mini-Reviewtissue-specific migration of T cells and the homing of DC to draining lymph nodes [4][5][6]. In combination with adhesion molecules, the homeostatic chemokines can form part of a very spec...

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DNA Microarray Gene Expression Profile of Marginal Zone versus Follicular B Cells and Idiotype Positive Marginal Zone B Cells before and after Immunization with Streptococcus pneumoniae

Cited by 49 publications

References 45 publications

Impaired B Cell Development in the Absence of Krüppel-like Factor 3

Impaired B Cell Development in the Absence of Krüppel-like Factor 3

Programming of marginal zone B-cell fate by basic Krüppel-like factor (BKLF/KLF3)

D6 and the atypical chemokine receptor family: Novel regulators of immune and inflammatory processes

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