Adaptive Immune Response in JAM-C-Deficient Mice: Normal Initiation but Reduced IgG Memory

Zimmerli, Claudia; Lee, Boris P.-L.; Palmer, Gaby; Gabay, Cem; Adams, Ralf H.; Aurrand-Lions, Michel; Imhof, Beat A.

doi:10.4049/jimmunol.0803892

Cited by 13 publications

(15 citation statements)

References 66 publications

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“…S5 C and D). The junctional cell adhesion molecule C (JAM-C) has been shown to direct transendothelial migration from the blood stream into B-cell follicles (52,53). Interestingly, IgG + B cells showed a biphasic expression of JAM-C, with about 50% of cells showing high levels, whereas the remaining cells had no detectable JAM-C surface expression (Fig.…”

Section: Coculture Of Igm Memory B Cells and Neutrophils Induces Pcmentioning

confidence: 99%

Functional capacities of human IgM memory B cells in early inflammatory responses and secondary germinal center reactions

Seifert

Przekopowitz

Taudien

et al. 2015

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

180

197

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The generation and functions of human peripheral blood (PB) IgM CD27+ B cells to migrate to B-cell follicles and undergo germinal center (GC) B-cell differentiation, whereas activated IgG + memory B cells preferentially showed a plasma cell (PC) fate. This observation was supported by reverse regulation of B-cell lymphoma 6 and PR domain containing 1 and differential BTB and CNC homology 1, basic leucine zipper transcription factor 2 expression. Moreover, IgM

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Section: Coculture Of Igm Memory B Cells and Neutrophils Induces Pcmentioning

confidence: 99%

Functional capacities of human IgM memory B cells in early inflammatory responses and secondary germinal center reactions

Seifert

Przekopowitz

Taudien

et al. 2015

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

180

197

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“…Although the JAM s are known to be expressed during embryogenesis, no developmental function has been described in the various mouse models to date [20], [25], [26], [36]–[40]. Our recent work on cell surface protein interactions identified a function for zebrafish orthologues of JAM-B and JAM-C (named Jamb and Jamc, respectively) in myogenesis [41].…”

Section: Introductionmentioning

confidence: 99%

Genomic Organisation, Embryonic Expression and Biochemical Interactions of the Zebrafish Junctional Adhesion Molecule Family of Receptors

Powell

Wright

2012

PLoS ONE

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The mammalian JAM family is composed of three cell surface receptors. Interactions between the proteins have well-characterised roles in inflammation and tight junction formation, but little is known about their function in early development. Recently, we identified a role for jamb and jamc in zebrafish myocyte fusion. Genome duplication in the teleost lineage raised the possibility that additional JAM family paralogues may also function in muscle development. To address this, we searched the zebrafish genome to identify potential paralogues and confirmed their homology, bringing the total number of zebrafish jam family members to six. We then compared the physical binding properties of each paralogue by surface plasmon resonance and determined the gene expression patterns of all zebrafish jam genes at different stages of development. Our results suggest a significant sub-functionalisation of JAM-B and JAM-C orthologues with respect to binding strength (but not specificity) and gene expression. The paralogous genes, jamb2 and jamc2, were not detected in the somites or myotome of wild-type embryos. We conclude that it is unlikely that the paralogues have a function in primary myogenesis.

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“…29 Because jam-c deficient males are infertile, the colony is maintained by interbreeding of jam-c ϩ/Ϫ mice maintained and back-crossed for Ͼ 8 generations on C57Bl/6 background. C57BL/6 and C57BL/6-CD45.1 were purchased from Janvier Laboratory and Charles River Laboratories, respectively.…”

Section: Micementioning

confidence: 99%

JAM-B regulates maintenance of hematopoietic stem cells in the bone marrow

Arcangeli

Frontera

Bardin

et al. 2011

Blood

Self Cite

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IntroductionThe junctional adhesion molecules (JAMs) are a subset of the immunoglobulin (Ig) protein superfamily and are characterized by the presence of both a type V and a type C2 extracellular Ig domain. JAMs and related molecules have been involved in the control of interendothelial junctions and leukocyte transendothelial migration through homotypic and heterotypic interactions. 1-5 JAM-B has been previously shown to interact with JAM-C and contributes to leukoendothelial and interendothelial cell-cell adhesion. 6,7 In mice, JAM-B expression is restricted to endothelial cells whereas JAM-C is expressed by various cell types including endothelial, 1,2 fibroblastic, 8 and smooth muscle cells. 9 Moreover, we have recently shown that JAM-C expression in lymph node fibroblastic cells is required for constitutive secretion of several chemokines such as SDF-1␣. 10 Recently, expression of several JAM family members, such as JAM-A, JAM-C, JAM4, or ESAM, has been reported in hematopoietic stem cells (HSCs), although a function for these proteins in hematopoiesis remains unknown. [11][12][13][14][15][16] In adult mammals, HSCs are rare cells mainly located in the bone marrow (BM) and able to generate all mature blood cells. In mice, HSCs are comprised within the LSK compartment as defined by the Lineage Neg c-kit Hi Sca-1 Hi (LSK) phenotype; the LSK compartment can be further subdivided using additional markers such as CD34, CD150, or CD48. Indeed, CD34 Neg CD135 Neg LSK, or Thy-1 Lo LSK 17,18 and CD150 Pos CD48 Neg LSK cells 19 have been shown to contain, respectively, around 20% and 50% of HSCs with long-term hematopoietic reconstitution potential (LT-HSCs). Because HSCs give rise to mature hematopoietic cells, including immune cells, their replacement must be adjusted to homeostatic or stress conditions such as infections, inflammation, or blood loss, and their expansion must be controlled to avoid exhaustion through inappropriate proliferation and differentiation. This is possible by the coordinated regulation of quiescence, self-renewal, and differentiation of HSCs through appropriate signals delivered by functional microenvironments called niches. [20][21][22] HSCs are restrained in these specialized microenvironments by interactions mediated by adhesion molecules and chemokine receptors expressed by HSCs, such as VLA-4 or CXCR4, with their ligands present within the BM microenvironment. Other signaling pathways controlled by growth factors and their receptors expressed on HSCs, such as angiopoietin-1 and TIE2, SCF and KIT, Thrombopoietin and MPL, have also been involved in HSC maintenance and retention in BM niches. 23,24 Whether the JAM family members expressed on HSCs also contribute to this signaling network has not been addressed so far.When necessary, HSCs enter the cell cycle to maintain BM cellularity and replenish peripheral blood in a process called mobilization, which can be induced using various hematopoietic growth factors, cyclophosphamide in combination with G-CSF (Cy/G-CSF), or intravenous inject...

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Adaptive Immune Response in JAM-C-Deficient Mice: Normal Initiation but Reduced IgG Memory

Cited by 13 publications

References 66 publications

Functional capacities of human IgM memory B cells in early inflammatory responses and secondary germinal center reactions

Functional capacities of human IgM memory B cells in early inflammatory responses and secondary germinal center reactions

Genomic Organisation, Embryonic Expression and Biochemical Interactions of the Zebrafish Junctional Adhesion Molecule Family of Receptors

JAM-B regulates maintenance of hematopoietic stem cells in the bone marrow

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