Immunological Memory: Contribution of Memory B Cells Expressing Costimulatory Molecules in the Resting State

Bar‐Or, Amit; Oliveira, Enedina Maria Lobato de; Anderson, David E.; Krieger, Jeffrey; Duddy, Martin; O’Connor, Kevin; Hafler, David A.

doi:10.4049/jimmunol.167.10.5669

Cited by 126 publications

(91 citation statements)

References 54 publications

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“…Previous studies showed that memory B cells differ from naïve cells in several aspects, including their size, Ig mRNA levels, response to in vitro activation stimuli, expression of the tumor necrosis factor receptor family member CD27 (18,20,29,45,46), and expression of CD80 and CD11b on a subset of cells (28). Our results confirm these few known differences, but indicate that the overall gene expression profiles of naïve and memory B cells are remarkably similar (Fig.…”

Section: Memory B Cellssupporting

confidence: 80%

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Transcriptional analysis of the B cell germinal center reaction

Klein

Stolovitzky

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

366

354

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Section: Memory B Cellssupporting

confidence: 80%

“…Among the adhesionassociated molecules, the CD11b͞Mac-1͞complement receptor type 3 gene was found to be strongly up-regulated in the CC 3 memory B cell transition (12.5-fold o.b. ); CD11b was recently shown to be expressed on a subpopulation of human peripheral blood memory B cells (28).…”

Section: Resultsmentioning

confidence: 99%

Transcriptional analysis of the B cell germinal center reaction

Klein

Stolovitzky

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

366

354

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“…A recent study showed that memory B cells expressing CD80 are able to secrete particularly large amounts of class-switched Ig, and can efficiently and rapidly present antigen to T cells and activate them (33). Therefore, the increase in CD80ϩ memory B cells in SSc may be responsible for the augmented IgG production by the memory B cells.…”

Section: Discussionmentioning

confidence: 99%

Altered blood B lymphocyte homeostasis in systemic sclerosis: Expanded naive B cells and diminished but activated memory B cells

Sato¹,

Fujimoto²,

Hasegawa³

et al. 2004

Arthritis & Rheumatism

281

205

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Objective. To determine phenotypic and functional abnormalities of blood B cell subsets in patients with systemic sclerosis (SSc).Methods. Cell surface marker expression was determined by flow cytometry. Spontaneous apoptosis was evaluated by annexin V expression with flow cytometric analysis. IgG production by isolated IgD؊ memory B cells was examined by enzyme-linked immunosorbent assay.Results

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“…17), and the mechanisms underlying B cell migration into the CNS have not been examined. Circulating human B cells are known to constitutively express the adhesion molecules VLA-4 and LFA-1 (37). The counterreceptors for these (VCAM-1 and ICAM-1, respectively) have been found up-regulated on BBB endothelial cells in MS lesions, at sites of B cell infiltration (38).…”

mentioning

confidence: 99%

Determinants of Human B Cell Migration Across Brain Endothelial Cells

Alter

Duddy

Hebert

et al. 2003

The Journal of Immunology

Self Cite

171

123

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Circulating B cells enter the CNS as part of normal immune surveillance and in pathologic states, including the common and disabling illness multiple sclerosis. However, little is known about the molecular mechanisms that mediate human B cell interaction with the specialized brain endothelial cells comprising the blood-brain barrier (BBB). We studied the molecular mechanisms that regulate the migration of normal human B cells purified ex vivo, across human adult brain-derived endothelial cells (HBECs). We found that B cells migrated across HBECs more efficiently than T cells from the same individuals. B cell migration was significantly inhibited by blocking Abs to the adhesion molecules ICAM-1 and VLA-4, but not VCAM-1, similar to the results previously reported for T cells. Blockade of the chemokines monocyte chemoattractant protein-1 and IL-8, but not RANTES or IFN-γ-inducible protein-10, significantly inhibited B cell migration, and these results were correlated with the chemokine receptor expression of B cells measured by flow cytometry and by RNase protection assay. Tissue inhibitor of metalloproteinase-1, a natural inhibitor of matrix metalloproteinases, significantly decreased B cell migration across the HBECs. A comprehensive RT-PCR comparative analysis of all known matrix metalloproteinases and tissue inhibitors of metalloproteinases in human B and T cells revealed distinct profiles of expression of these molecules in the different cell subsets. Our results provide insights into the molecular mechanisms that underlie human B cell migration across the BBB. Furthermore, they identify potential common, and unique, therapeutic targets for limiting CNS B cell infiltration and predict how therapies currently developed to target T cell migration, such as anti-VLA-4 Abs, may impact on B cell trafficking.

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Immunological Memory: Contribution of Memory B Cells Expressing Costimulatory Molecules in the Resting State

Cited by 126 publications

References 54 publications

Transcriptional analysis of the B cell germinal center reaction

Transcriptional analysis of the B cell germinal center reaction

Altered blood B lymphocyte homeostasis in systemic sclerosis: Expanded naive B cells and diminished but activated memory B cells

Determinants of Human B Cell Migration Across Brain Endothelial Cells

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