Swiprosin-1/EFhd2 Controls B Cell Receptor Signaling through the Assembly of the B Cell Receptor, Syk, and Phospholipase C γ2 in Membrane Rafts

Kroczek, Carmen; Lang, Caroline; Brachs, Sebastian; Grohmann, Marcus; Dütting, Sebastian; Schweizer, Astrid; Nitschke, Lars; Feller, Stephan M.; Jäck, Hans‐Martin; Mielenz, Dirk

doi:10.4049/jimmunol.0903642

Cited by 53 publications

(79 citation statements)

References 80 publications

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“…Additionally, cytokine secretion in human mast cells is thought to be guided by swip-1/EFHD2 (Ramesh et al, 2009). Hemocytes, macrophage-like cells of the invertebrate innate immune system, are known to transcribe CG10641 (Estrada et al, 2006; Kroczek et al, 2010) and our study found a polar distribution of Drosophila Swip-1 in the macrophage-like hemocytes of the embryo. Taken together, these findings suggest a conserved function of swiprosin in the innate immune system of invertebrates and vertebrates.…”

Section: Discussionsupporting

confidence: 59%

“…Thus, in many aspects, the Drosophila protein is highly conserved with mammalian swiprosins (Fig. 1), and therefore, we named the CG10641 protein Drosophila Swip-1 in accordance with Kroczek and colleagues (Kroczek et al, 2010).…”

Section: Resultsmentioning

confidence: 99%

“…Interestingly, the FCM-specific protein Blow, a putative regulator of F-actin and Kette (Kesper et al, 2007;Richardson et al, 2007;Schröter et al, 2006) also accumulates in a similar manner to Swip-1. In human mast cells, EFHD2/swiprosin-1 was shown to colocalise to the actin-cytoskeleton (Kroczek et al, 2010;Ramesh et al, 2009). This raises the question of whether Drosophila Swip-1 is a regulator of F-actin on the side of the FCMs.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, Swiprosin-1/EFHD2 is thought to control B-cellreceptor signalling in mouse (Kroczek et al, 2010) and cytokine expression in human mast cells (Ramesh et al, 2009;Thylur et al, 2009), and it is also known to be present in human cytotoxic lymphocytes (Vuadens et al, 2004).…”

Section: The Progression From Prefusion Complex To Membrane Breakdownmentioning

confidence: 99%

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Drosophila Swiprosin-1/EFHD2 accumulates at the prefusion complex stage during Drosophila myoblast fusion

Hornbruch-Freitag¹,

Griemert²,

Buttgereit³

et al. 2011

Development

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Section: Discussionsupporting

confidence: 59%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: The Progression From Prefusion Complex To Membrane Breakdownmentioning

confidence: 99%

See 2 more Smart Citations

Drosophila Swiprosin-1/EFHD2 accumulates at the prefusion complex stage during Drosophila myoblast fusion

Hornbruch-Freitag¹,

Griemert²,

Buttgereit³

et al. 2011

Development

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“…Calcium flux measurements were performed as described (42,43 was restored after 240 s. Changes in Indo-1 AM fluorescence ratios were analyzed in gated FO and MZ B cell populations with a LSRII flow cytometer (BD Biosciences) using FlowJo software (Tree Star). Equal Indo-1 loading was assessed by ionomycin stimulation.…”

Section: Methodsmentioning

confidence: 99%

B cell homeostasis and plasma cell homing controlled by Krüppel-like factor 2

Winkelmann

Sandrock²,

Porstner³

et al. 2010

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

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118

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Krüppel-like factor 2 (KLF2) controls T lymphocyte egress from lymphoid organs by regulating sphingosin-1 phosphate receptor 1 (S1Pr1). Here we show that this is not the case for B cells. Instead, KLF2 controls homeostasis of B cells in peripheral lymphatic organs and homing of plasma cells to the bone marrow, presumably by controlling the expression of β 7 -integrin. In mice with a B cell-specific deletion of KLF2, S1Pr1 expression on B cells was only slightly affected. Accordingly, all splenic B cell subsets including B1 cells were present, but their numbers were increased with a clear bias for marginal zone (MZ) B cells. In contrast, fewer peyers patches harboring fewer B cells were found, and fewer B1 cells in the peritoneal cavity as well as recirculating B cells in the bone marrow were detected. Upon thymus-dependent immunization, IgG titers were diminished, and antigen-specific plasma cells were absent in the bone marrow, although numbers of antigen-specific splenic plasmablasts were normal. KLF2 plays also a role in determining the identity of follicular B cells, as KLF2-deficient follicular B cells showed calcium responses similar to those of MZ B cells and failed to down-regulate MZ B cell signature genes, such as CD21 and CXCR7.cell trafficking | S1P1 | LKLF | B cell development | knockout mouse M aturation of lymphocytes in primary lymphoid organs, controlled egress into the periphery, and proper positioning in lymphoid tissues are critical for efficient adaptive immune responses. Differential expression of Krüppel-like factor 2 (KLF2) promotes egress of T cells from lymphoid organs into the blood and T-cell migration to lymph nodes (1, 2). Accordingly, KLF2 is expressed in naive T cells, down-regulated upon activation, and reexpressed in memory T cells (1, 3-5). KLF2-deficient T cells inefficiently exit from the thymus and thus accumulate there; this is thought to be a consequence of a decrease in sphingosin-1 phosphate receptor 1 (S1Pr1) expression, which is regulated by KLF2 (2, 6). In addition, KLF2 increases the expression of β 7 -integrin (gene symbol: Itgb7) and CD62L (L-selectin) on T cells (1, 2). However, other downstream effects of KLF2 expression are less clear, although they very likely contribute to the migratory behavior of T cells. For example, vav-cre-and lck-cre-mediated deletion of KLF2 in T cells resulted in the up-regulation of the inflammatory chemokine receptors CCR3 and CCR5 (7) on thymocytes, whereas CD4-cre-mediated deletion led to the up-regulation of only CXCR3 and spontaneous IL4 production in naive T cells (8).Although the role of KLF2 in T-cell migration has been studied extensively, its function in B cells is not fully understood. KLF2 expression at the RNA and protein level is induced by pre-B cell receptor (pre-BCR) signals (9). Analogous to T cells, KLF2 transcripts are abundant in resting mature B cells, down-regulated upon mitogenic activation, and reexpressed in plasma and memory B cells (10)(11)(12). Because KLF2 controls the expression of β 7 -integrin and CD62...

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