46 research outputs found

    Dispersive hydrodynamics of nonlinear polarization waves in two-component Bose-Einstein condensates

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    We study one dimensional mixtures of two-component Bose-Einstein condensates in the limit where the intra-species and inter-species interaction constants are very close. Near the mixing-demixing transition the polarization and the density dynamics decouple. We study the nonlinear polarization waves, show that they obey a universal (i.e., parameter free) dynamical description, identify a new type of algebraic soliton, explicitly write simple wave solutions, and study the Gurevich-Pitaevskii problem in this context

    Topological constraints on the dynamics of vortex formation in a bi-dimensional quantum fluid

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    We present experimental and theoretical results on formation of quantum vortices in a laser beam propagating in a nonlinear medium. Topological constrains richer that the mere conservation of vorticity impose an elaborate dynamical behavior to the formation and annihilation of vortex/anti-vortex pairs. We identify two such mechanisms, both described by the same fold-Hopf bifurcation. One of them is particularly efficient although it is not observed in the context of liquid helium films or stationary linear systems because it relies on the finite compressibility and on the non-stationnarity of the fluid of light we consider

    The FcyRIIIa/CD16a receptor importance among the activating receptors of Natural Killer (NK) cells : cellular expression and functional responses triggered by its engagement.

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    Les cellules NK sont capables d’ADCC (Antibody Dependent Cytotoxicity) suite Ă  l’engagement durĂ©cepteur Fc!RIIIa/CD16a, et de fonctions effectrices directes antivirales et anti-tumorales: c’est la«cytotoxicitĂ© naturelle ». Ainsi activĂ©es elles peuvent Ă©galement rĂ©pondre en produisant des cytokines, commel’IFN-!. La dĂ©granulation et la synthĂšse d’IFN-! par les cellules NK observĂ©es aprĂšs engagement du rĂ©cepteurCD16a, dont l’expression est indĂ©pendante du polymorphisme V158F, ont Ă©tĂ© largement supĂ©rieures Ă  cellesobtenues avec les autres rĂ©cepteurs activateurs. Son engagement par les AcMor thĂ©rapeutiques a produit desrĂ©ponses fonctionnelles variables selon l’AcMor, et selon les donneurs de cellules. La perte d’expression duCD16a membranaire s’est rĂ©vĂ©lĂ© ĂȘtre un marqueur sensible de l’activation des cellules NK, mĂȘme quand cedernier n’était pas engagĂ©. Enfin, l’emploi de d’inhibiteur d’ADAM17 (TMI-2 et TIMP3) a permis d’observerle maintien de l’expression du CD16a aprĂšs activation cellulaire sans augmenter les rĂ©ponses fonctionnelles.Ce travail souligne la place centrale de l’engagement du CD16a dans l’activation NK.NK cell can trigger ADCC (Antibody Dependent Cytotoxicity) through the engagement of theFc!RIIIa/CD16a receptor, and « Natural Cytotoxicity » after integration of cellular signals coming from theiractivating and inhibitory receptors. Moreover, activated NK cells produce cytokines such as IFN-!.Engagement by monoclonal antibodies (mAb) of CD16a was strongly more efficient than that of any otheractivating receptor to induce degranulation and IFN-! synthesis. Functional responses depend on thetherapeutic mAb used to engage CD16a and on the donor of NK cells. CD16a down-modulation was a verysensitive marker of NK cell activation, whatever the mean of activation. It was inhibited in the presence ofTMI-2 and TIMP3 (ADAM17 inhibitors), whereas CD16-dependent functional responses were not increased.This work highlighted the major role of the CD16a receptor in the activation of NK cells

    RÎle majeur du FcyRIIIa/CD16a parmi les récepteurs activateurs des cellules tueuses naturelles (cellules NK) (etude de son expression et des réponses fonctionnelles induites par son engagement.)

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    Les cellules NK sont capables d ADCC (Antibody Dependent Cytotoxicity) suite Ă  l engagement durĂ©cepteur Fc!RIIIa/CD16a, et de fonctions effectrices directes antivirales et anti-tumorales: c est la cytotoxicitĂ© naturelle . Ainsi activĂ©es elles peuvent Ă©galement rĂ©pondre en produisant des cytokines, commel IFN-!. La dĂ©granulation et la synthĂšse d IFN-! par les cellules NK observĂ©es aprĂšs engagement du rĂ©cepteurCD16a, dont l expression est indĂ©pendante du polymorphisme V158F, ont Ă©tĂ© largement supĂ©rieures Ă  cellesobtenues avec les autres rĂ©cepteurs activateurs. Son engagement par les AcMor thĂ©rapeutiques a produit desrĂ©ponses fonctionnelles variables selon l AcMor, et selon les donneurs de cellules. La perte d expression duCD16a membranaire s est rĂ©vĂ©lĂ© ĂȘtre un marqueur sensible de l activation des cellules NK, mĂȘme quand cedernier n Ă©tait pas engagĂ©. Enfin, l emploi de d inhibiteur d ADAM17 (TMI-2 et TIMP3) a permis d observerle maintien de l expression du CD16a aprĂšs activation cellulaire sans augmenter les rĂ©ponses fonctionnelles.Ce travail souligne la place centrale de l engagement du CD16a dans l activation NK.NK cell can trigger ADCC (Antibody Dependent Cytotoxicity) through the engagement of theFc!RIIIa/CD16a receptor, and Natural Cytotoxicity after integration of cellular signals coming from theiractivating and inhibitory receptors. Moreover, activated NK cells produce cytokines such as IFN-!.Engagement by monoclonal antibodies (mAb) of CD16a was strongly more efficient than that of any otheractivating receptor to induce degranulation and IFN-! synthesis. Functional responses depend on thetherapeutic mAb used to engage CD16a and on the donor of NK cells. CD16a down-modulation was a verysensitive marker of NK cell activation, whatever the mean of activation. It was inhibited in the presence ofTMI-2 and TIMP3 (ADAM17 inhibitors), whereas CD16-dependent functional responses were not increased.This work highlighted the major role of the CD16a receptor in the activation of NK cells.TOURS-Bibl.Ă©lectronique (372610011) / SudocSudocFranceF

    Gradual Increase of FcÎłRIIIa/CD16a Expression and Shift toward IFN-Îł Secretion during Differentiation of CD56dim Natural Killer Cells

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    Natural killer (NK) cell effector functions include cytotoxicity and secretion of cytokines such as interferon-γ (IFN-γ). The immature CD56bright subset of human NK cells lacks expression of FcγRIIIa/CD16a, one of the low-affinity immunoglobulin G receptors, or exhibits low-density expression (CD56brightCD16−/dim) and produces IFN-γ in response to cytokine stimulation, whereas the mature CD56dimCD16+ subset is the most cytotoxic one. A further differentiation/maturation of the latter subset according to the gradual loss of NKG2A and/or gain of KIR2DL (CD158a and CD158b) has been demonstrated and the ability to produce IFN-γ in response to activating receptor (AR) co-engagement is gradually acquired during terminal differentiation. In the course of flow cytometry analysis of CD56dim NK cells, we noted a substantial intraindividual heterogeneity of expression of FcγRIIIa. FcγRIIIa is unique among ARs: it does not require the co-engagement of other ARs to induce substantial cytotoxicity or cytokine synthesis in CD56dim cells. We, therefore, investigated whether individual differentiation/maturation of polyclonal CD56dim NK cells defined by expression of NKG2A/KIR2DL is related to FcγRIIIa expression and to the heterogeneity of NK cell responses upon FcγRIIIa engagement. When we analyzed unstimulated CD56dim cells by increasing level of FcγRIIIa expression, we found that the proportion of the more differentiated CD158a,h+ and/or CD158b,j+ cells and that of the less differentiated NKG2A+ cells gradually increased and decreased, respectively. FcγRIIIa engagement by using plate-bound murine anti-CD16 monoclonal antibody (mAb) or rituximab or trastuzumab (two therapeutic mAbs), resulted in donor-dependent partial segregation of IFN-γ-producing and/or degranulating CD56dim cells. Importantly, the proportion of CD158a,h/b,j+ cells and that of NKG2A+ cells was increased and decreased, respectively, IFN-γ-producing cells, whereas these proportions were poorly modified in degranulating cells. Similar results were observed after engagement of ARs by a combination of mAbs targeting NKG2D, NKp30, NKp46, and 2B4. Thus, the gradual increase of FcγRIIIa expression is an important feature of the differentiation/maturation of CD56dim cells and this differentiation/maturation is associated with a shift in functionality toward IFN-γ secretion observed upon both FcγRIIIa-dependent and FcγRIIIa-independent stimulation. The functional heterogeneity related to the differentiation/maturation of CD56dim NK cells could be involved in the variability of the clinical responses observed in patients treated with therapeutic mAbs

    Identification of the novel HLA‐DRB3 *02:174 allele by next‐generation sequencing

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    International audienceHLA-DRB3*02:174 differs from DRB3*02:02:01 by one nucleotide substitution in codon 95 in exon 3

    Identification of the novel HLA‐DRB1 *04:335 allele by next‐generation sequencing

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    International audienceHLA-DRB1*04:335 differs from DRB1*04:01:01 by one nucleotide substitution in codon 28 in exon 2. This article is protected by copyright. All rights reserved

    Identification of the novel HLA‐DQA1 *01:82 allele by next‐generation sequencing

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    International audienceHLA-DQA1*01:82 differs from DQA1*01:03:01 by one nucleotide substitution in codon 49 in exon 2. This article is protected by copyright. All rights reserved

    Identification of the novel HLA‐DQB1 *03:471 allele by next‐generation sequencing

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    International audienceHLA-DQB1*03:471 differs from DQB1*03:02:01 by one nucleotide substitution in codon 142 in exon 3
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