Down modulation of L‐Selectin expression on eosinophils recovered from bronchoalveolar lavage fluid after allergen provocation

Mengelers, H. J. J.; Maikoe, Tjander; Hooibrink, Berend; Kuypers, T.W.; Kreukniet, J.; Lammers, Jan-Willem; Koenderman, Leo

doi:10.1111/j.1365-2222.1993.tb00882.x

Cited by 36 publications

(19 citation statements)

References 41 publications

(57 reference statements)

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“…These data suggest that expression of am/CD11b and L-selectin/CD62L is controlled differently compared with the modulated expression of these markers on cells activated in vitro (Fig 1, F) 39,40 or in the lung tissue in vivo. 47 Our data are consistent with a model that am bright /L-selectin bright cells comprise a phenotype that facilitates adhesion and homing in allergic asthmatic subjects. During subsequent extravasation, Lselectin is shed from the surface, whereas am is even more increased.…”

Section: Discussionsupporting

confidence: 91%

Expression of activated FcγRII discriminates between multiple granulocyte-priming phenotypes in peripheral blood of allergic asthmatic subjects

Kanters

Hove

Luijk

et al. 2007

Journal of Allergy and Clinical Immunology

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Section: Discussionsupporting

confidence: 91%

Expression of activated FcγRII discriminates between multiple granulocyte-priming phenotypes in peripheral blood of allergic asthmatic subjects

Kanters

Hove

Luijk

et al. 2007

Journal of Allergy and Clinical Immunology

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“…CD29 is a member of the very-late-activation integrin family and known to function as an adhesion and signaling molecule. CD62L (L-selectin) plays a critical role in initiating the interactions of cells with the activated endothelium at an inflammatory site and is characteristically down-modulated in response to cell activation (6,16,19). Increased CD29 and decreased CD62L levels were also observed in the present study after eosinophils were exposed to S. stercoralis antigens.…”

Section: Discussionsupporting

confidence: 64%

Eosinophils Can Function as Antigen-Presenting Cells To Induce Primary and Secondary Immune Responses toStrongyloides stercoralis

et al. 2006

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Several studies have demonstrated roles for eosinophils during innate and adaptive immune responses to helminth infections. However, evidence that eosinophils are capable of initiating an immune response to parasite antigens is lacking. The goal of the present in vitro study was to investigate the potential of eosinophils to serve as antigen-presenting cells (APC) and initiate an immune response to parasite antigens. Purified eosinophils were exposed to soluble Strongyloides stercoralis antigens, and the expression of various surface markers involved in cell activation was examined. Antigen-exposed eosinophils showed a sixfold increase in expression levels of CD69 and major histocompatibility complex (MHC) class II, a fourfold increase in levels of T-cell costimulatory molecule CD86, and a twofold decrease in levels of CD62L compared to eosinophils cultured in medium containing granulocyte-macrophage colony-stimulating factor. The ability of eosinophils to present antigen to T cells was determined by culturing them with T cells in vitro. Eosinophils pulsed with antigen stimulated antigen-specific primed T cells and CD4 ؉ T cells to increase interleukin-5 (IL-5) production. The blocking of MHC class II expression on eosinophils inhibited their ability to induce IL-5 production by CD4؉ T cells in culture. Antigen-pulsed eosinophils were able to prime naïve T cells and CD4 ؉ T cells in culture and polarized them into Th2 cells producing IL-5 similar to that induced by antigen-loaded dendritic cells. These results demonstrate that eosinophils are capable of activating antigen-specific Th2 cells inducing the release of cytokines and assist in the priming of naïve T cells to initiate Th2 responses against infection. This study highlights the potential of eosinophils to actively induce immune responses against infection by amplifying antigen-specific Th2-cell responses.

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“…One of the activating agents produced by endothelial cells is platelet-activating factor (PAF) [11]. The increase of CD11b expression and concomitant shedding of L-selectin is not only observed in vitro [12,13]; a number of studies have shown increased Mac-1 expression and decreased L-selectin expression on extravasated neutrophils and eosinophils in vivo [2,14,15].…”

mentioning

confidence: 99%

Inhibition of PAF-induced expression of CD11b and shedding of L-selectin on human neutrophils and eosinophils by the type IV selective PDE inhibitor, rolipram

Berends¹,

Dijkhuizen²,

Monchy

et al. 1997

Eur Respir J

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We quantitatively determined whether the selective phosphodiesterase (PDE) inhibitor, rolipram, inhibits changes in the adhesion molecules CD11b and L-selectin on platelet-activating factor (PAF)-stimulated human neutrophils and eosinophils in vitro.Incubations were performed in human whole blood obtained from healthy volunteers, to restrict activation by purification procedures and to simulate in vivo conditions, in which different cell types may interact, more closely. Receptor expression was measured after fixation of cells, using monoclonal antibodies and flow cytometry.Concentration-dependent inhibition of the PAF-induced CD11b expression and L-selectin shedding for neutrophils and eosinophils was observed with rolipram, dibutyryl cyclic adenosine monophosphate (cAMP), prostaglandin E 2 (PGE 2 ), and isoproterenol. However, these inhibitions did not exceed 50%. Preincubation with rolipram (10 -8 M) and subsequent incubation with isoproterenol (0.5×10 -8 M) or PGE 2 (10 -8 M) induced a cumulative, but not synergistic, effect. Using the combination of rolipram with isoproterenol or PGE 2 , inhibition of PAF-induced Lselectin shedding from eosinophils was as high as 71±28 and 67±21%, respectively. Other inhibitions were below 50%.In conclusion, rolipram inhibits CD11b expression and L-selectin shedding of platelet-activating factor-stimulated neutrophils and eosinophils in whole blood in a concentration-dependent fashion. Inhibitions did not exceed 50%, even at high concentrations. The inhibition of platelet-activating factor induced shedding of Lselectin from eosinophils with a combination of rolipram and prostaglandin E 2 or isoproterenol, however, was found to be approximately 70%. Inhibition of rolling adhesion of eosinophils may, therefore, be a mode of action of type IV phosphodiesterase inhibitors.

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Down modulation of L‐Selectin expression on eosinophils recovered from bronchoalveolar lavage fluid after allergen provocation

Cited by 36 publications

References 41 publications

Expression of activated FcγRII discriminates between multiple granulocyte-priming phenotypes in peripheral blood of allergic asthmatic subjects

Expression of activated FcγRII discriminates between multiple granulocyte-priming phenotypes in peripheral blood of allergic asthmatic subjects

Eosinophils Can Function as Antigen-Presenting Cells To Induce Primary and Secondary Immune Responses toStrongyloides stercoralis

Inhibition of PAF-induced expression of CD11b and shedding of L-selectin on human neutrophils and eosinophils by the type IV selective PDE inhibitor, rolipram

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