The target asymmetry
T
, recoil asymmetry
P
, and beam-target double polarization observable
H
were determined in exclusive
π
0
and
η
photoproduction off quasi-free protons and, for the first time, ...off quasi-free neutrons. The experiment was performed at the electron stretcher accelerator ELSA in Bonn, Germany, with the Crystal Barrel/TAPS detector setup, using a linearly polarized photon beam and a transversely polarized deuterated butanol target. Effects from the Fermi motion of the nucleons within deuterium were removed by a full kinematic reconstruction of the final state invariant mass. A comparison of the data obtained on the proton and on the neutron provides new insight into the isospin structure of the electromagnetic excitation of the nucleon. Earlier measurements of polarization observables in the
γ
p
→
π
0
p
and
γ
p
→
η
p
reactions are confirmed. The data obtained on the neutron are of particular relevance for clarifying the origin of the narrow structure in the
η
n
system at
W
=
1.68
GeV
. A comparison with recent partial wave analyses favors the interpretation of this structure as arising from interference of the
S
11
(
1535
)
and
S
11
(
1650
)
resonances within the
S
11
-partial wave.
Abstract
The target asymmetry
T
, recoil asymmetry
P
, and beam-target double polarization observable
H
were determined in exclusive
$$\pi ^0$$
π
0
and
$$\eta $$
η
photoproduction off quasi-free ...protons and, for the first time, off quasi-free neutrons. The experiment was performed at the electron stretcher accelerator ELSA in Bonn, Germany, with the Crystal Barrel/TAPS detector setup, using a linearly polarized photon beam and a transversely polarized deuterated butanol target. Effects from the Fermi motion of the nucleons within deuterium were removed by a full kinematic reconstruction of the final state invariant mass. A comparison of the data obtained on the proton and on the neutron provides new insight into the isospin structure of the electromagnetic excitation of the nucleon. Earlier measurements of polarization observables in the
$$\gamma p \rightarrow \pi ^0 p$$
γ
p
→
π
0
p
and
$$\gamma p \rightarrow \eta p$$
γ
p
→
η
p
reactions are confirmed. The data obtained on the neutron are of particular relevance for clarifying the origin of the narrow structure in the
$$\eta n$$
η
n
system at
$$W = 1.68\ \textrm{GeV}$$
W
=
1.68
GeV
. A comparison with recent partial wave analyses favors the interpretation of this structure as arising from interference of the
$$S_{11}(1535)$$
S
11
(
1535
)
and
$$S_{11}(1650)$$
S
11
(
1650
)
resonances within the
$$S_{11}$$
S
11
-partial wave.
The target asymmetry
T
, recoil asymmetry
P
, and beam-target double polarization observable
H
were determined in exclusive
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\begin{document}$$\pi ^0$$\end{document}
π
0
and
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η
photoproduction off quasi-free protons and, for the first time, off quasi-free neutrons. The experiment was performed at the electron stretcher accelerator ELSA in Bonn, Germany, with the Crystal Barrel/TAPS detector setup, using a linearly polarized photon beam and a transversely polarized deuterated butanol target. Effects from the Fermi motion of the nucleons within deuterium were removed by a full kinematic reconstruction of the final state invariant mass. A comparison of the data obtained on the proton and on the neutron provides new insight into the isospin structure of the electromagnetic excitation of the nucleon. Earlier measurements of polarization observables in the
\documentclass12pt{minimal}
\usepackage{amsmath}
\usepackage{wasysym}
\usepackage{amsfonts}
\usepackage{amssymb}
\usepackage{amsbsy}
\usepackage{mathrsfs}
\usepackage{upgreek}
\setlength{\oddsidemargin}{-69pt}
\begin{document}$$\gamma p \rightarrow \pi ^0 p$$\end{document}
γ
p
→
π
0
p
and
\documentclass12pt{minimal}
\usepackage{amsmath}
\usepackage{wasysym}
\usepackage{amsfonts}
\usepackage{amssymb}
\usepackage{amsbsy}
\usepackage{mathrsfs}
\usepackage{upgreek}
\setlength{\oddsidemargin}{-69pt}
\begin{document}$$\gamma p \rightarrow \eta p$$\end{document}
γ
p
→
η
p
reactions are confirmed. The data obtained on the neutron are of particular relevance for clarifying the origin of the narrow structure in the
\documentclass12pt{minimal}
\usepackage{amsmath}
\usepackage{wasysym}
\usepackage{amsfonts}
\usepackage{amssymb}
\usepackage{amsbsy}
\usepackage{mathrsfs}
\usepackage{upgreek}
\setlength{\oddsidemargin}{-69pt}
\begin{document}$$\eta n$$\end{document}
η
n
system at
\documentclass12pt{minimal}
\usepackage{amsmath}
\usepackage{wasysym}
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\usepackage{amssymb}
\usepackage{amsbsy}
\usepackage{mathrsfs}
\usepackage{upgreek}
\setlength{\oddsidemargin}{-69pt}
\begin{document}$$W = 1.68\ \textrm{GeV}$$\end{document}
W
=
1.68
GeV
. A comparison with recent partial wave analyses favors the interpretation of this structure as arising from interference of the
\documentclass12pt{minimal}
\usepackage{amsmath}
\usepackage{wasysym}
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\setlength{\oddsidemargin}{-69pt}
\begin{document}$$S_{11}(1535)$$\end{document}
S
11
(
1535
)
and
\documentclass12pt{minimal}
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\usepackage{wasysym}
\usepackage{amsfonts}
\usepackage{amssymb}
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\begin{document}$$S_{11}(1650)$$\end{document}
S
11
(
1650
)
resonances within the
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\begin{document}$$S_{11}$$\end{document}
S
11
-partial wave.
Adaptive cellular immunity is initiated by antigen-specific interactions between T lymphocytes and dendritic cells (DCs). Plasmacytoid DCs (pDCs) support antiviral immunity by linking innate and ...adaptive immune responses. Here we examined pDC spatiotemporal dynamics during viral infection to uncover when, where, and how they exert their functions. We found that pDCs accumulated at sites of CD8+ T cell antigen-driven activation in a CCR5-dependent fashion. Furthermore, activated CD8+ T cells orchestrated the local recruitment of lymph node-resident XCR1 chemokine receptor-expressing DCs via secretion of the XCL1 chemokine. Functionally, this CD8+ T cell-mediated reorganization of the local DC network allowed for the interaction and cooperation of pDCs and XCR1+ DCs, thereby optimizing XCR1+ DC maturation and cross-presentation. These data support a model in which CD8+ T cells upon activation create their own optimal priming microenvironment by recruiting additional DC subsets to the site of initial antigen recognition.
Display omitted
•CXCR3 and CCR5 selectively control intranodal pDC migration•CD8+ T cells instruct pDC recruitment via CCL3 and CCL4•CD8+ T cells directly recruit XCR1+ DCs via XCL1•Active colocalization of XCR1+ DCs and pDCs supports DC cooperativity
pDCs and XCR1+ dendritic cells are critical for the generation of antiviral CD8+ T cell responses. Brewitz and colleagues demonstrate that primed CD8+ T cells reorganize the intranodal dendritic cell network to optimize pDC and XCR1+ DC cooperativity and thereby enhance CD8+ T cell immunity.
Inflammation and infection can trigger local tissue Na+ accumulation. This Na+-rich environment boosts proinflammatory activation of monocyte/macrophage-like cells (MΦs) and their antimicrobial ...activity. Enhanced Na+-driven MΦ function requires the osmoprotective transcription factor nuclear factor of activated T cells 5 (NFAT5), which augments nitric oxide (NO) production and contributes to increased autophagy. However, the mechanism of Na+ sensing in MΦs remained unclear. High extracellular Na+ levels (high salt HS) trigger a substantial Na+ influx and Ca2+ loss. Here, we show that the Na+/Ca2+ exchanger 1 (NCX1, also known as solute carrier family 8 member A1 SLC8A1) plays a critical role in HS-triggered Na+ influx, concomitant Ca2+ efflux, and subsequent augmented NFAT5 accumulation. Moreover, interfering with NCX1 activity impairs HS-boosted inflammatory signaling, infection-triggered autolysosome formation, and subsequent antibacterial activity. Taken together, this demonstrates that NCX1 is able to sense Na+ and is required for amplifying inflammatory and antimicrobial MΦ responses upon HS exposure. Manipulating NCX1 offers a new strategy to regulate MΦ function.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
To cite this article: Peng WM, Yu CF, Kolanus W, Mazzocca A, Bieber T, Kraft S, Novak N. Tetraspanins CD9 and CD81 are molecular partners of trimeric FcɛRI on human antigen‐presenting cells. Allergy ...2011; 66: 605–611.
Background: Most functions of tetraspanins are not related to cell‐surface receptor ligand binding, but are mediated by direct interactions with their partner proteins. Functions of trimeric FcɛRI, expressed by antigen‐presenting cells (APCs), range from amplification of allergic inflammatory reactions to their active suppression. Cell‐type‐specific protein–protein interactions might play a role in the regulation of these bidirectional tasks. Therefore, we intended to study the interactions of trimeric FcɛRI with tetraspanins.
Methods: The expression levels of tetraspanins CD9, CD37, CD53, CD63, CD81, CD82, and CD151 on skin dendritic cells of atopic dermatitis (AD) patients or healthy individuals were detected by flow cytometry. Tetraspanin expression on FcɛRIpos and FcɛRIneg monocyte subpopulations was evaluated. Flow cytometry, confocal microscopy, immunoprecipitation, and immunoblotting experiments were performed to observe the relationship between tetraspanins CD9 and CD81 and FcɛRI. Furthermore, plate stimulation experiments were performed, and cytokines in the supernatants were detected.
Results: We found that human FcɛRIpos APCs expressed high amounts of tetraspanins and that the tetraspanins CD9 and CD81 were associated with FcɛRI. Concomitant activation of FcɛRI and CD9 on human monocytes increased FcɛRI‐mediated cytokine release.
Conclusion: Taken together, we show for the first time that CD9 and CD81 act as molecular partners of trimeric FcɛRI on human APC, which might be of importance in allergic diseases such as AD.
During HIV/SIV infection, there is widespread programmed cell death in infected and, perhaps more importantly, uninfected cells. Much of this apoptosis is mediated by Fas-Fas ligand (FasL) ...interactions. Previously we demonstrated in macaques that induction of FasL expression and apoptotic cell death of both CD4(+) and CD8(+) T cells by SIV is dependent on a functional nef gene. However, the molecular mechanism whereby HIV-1 induces the expression of FasL remained poorly understood. Here we report a direct association of HIV-1 Nef with the zeta chain of the T cell receptor (TCR) complex and the requirement of both proteins for HIV-mediated upregulation of FasL. Expression of FasL through Nef depended upon the integrity of the immunoreceptor tyrosine-based activation motifs (ITAMs) of the TCR zeta chain. Conformation for the importance of zeta for Nef-mediated signaling in T cells came from an independent finding. A single ITAM motif of zeta but not CD3epsilon was both required and sufficient to promote activation and binding of the Nef-associated kinase (NAK/p62). Our data imply that Nef can form a signaling complex with the TCR, which bypasses the requirement of antigen to initiate T cell activation and subsequently upregulation of FasL expression. Thus, our study may provide critical insights into the molecular mechanism whereby the HIV-1 accessory protein Nef contributes to the pathogenesis of HIV.
Intracellular signaling pathways, which regulate the interactions of integrins with their ligands, affect a wide variety of biological functions. Here we provide evidence of how cytohesin‐1, an ...integrin‐binding protein and guanine‐nucleotide exchange factor (GEF) for ARF GTPases, regulates cell adhesion. Mutational analyses of the β‐2 cytoplasmic domain revealed that the adhesive function of LFA‐1 depends on its interaction with cytohesin‐1, unless the integrin is activated by exogenous divalent cations. Secondly, cytohesin‐1 induces expression of an extracellular activation epitope of LFA‐1, and the exchange factor function is not essential for this activity. In contrast, LFA‐1‐mediated cell adhesion and spreading on intercellular cell adhesion molecule 1 is strongly inhibited by a cytohesin‐1 mutant, which fails to catalyze ARF GDP–GTP exchange in vitro. Thus, cytohesin‐1 is involved in the activation of LFA‐1, most probably through direct interaction with the integrin, and induces cell spreading by its ARF‐GEF activity. We therefore propose that both direct regulation of the integrin and concomitant changes in the membrane topology of adherent T cells are modulated by dissectable functions of cytohesin‐1.
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