Inhibition of IgE binding to mast cells and basophils by monoclonal antibodies to murine IgE

Baniyash, Michal; Eshhar, Zelig

doi:10.1002/eji.1830140907

Cited by 126 publications

(68 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The detection limit of this ELISA was 0.2 ng/ ml, TNP-specific IgE was quantified in a modified sandwich ELiSA. Plates were coated with monoclonal RaAM/lgE (EM95, 2/xg/ml) [28] and incubated overnight at 4''C with diluted serum samples.…”

Section: Methodsmentioning

confidence: 99%

Prolonged In Vivo IL‐4 Treatment Inhibits Antigen‐Specific IgG1 and IgE Formation

1994

View full text Add to dashboard Cite

van Ommen R. Vredendaal AECM, Savelkoul HFJ. Prolonged In Vivo IL-4 Treatment Inhibits Antigen-Specific IgGi and IgE Formation. Scand J Immunol I994;40:l-9 IL-4 is obligatory for primary IgE responses, whereas primary IgGi and secondary IgE responses are partially IL-4 independent. To investigate the effect of IL-4 on the antigen-specific memory formation for these isotypes, BALB/c mice were treated after primary TNP-K.LH immunization with recombinant IL-4 for a period of 4 months. This prolonged presence of a high IL-4 level resulted in increased serum levels of total IgG, and IgE, whereas total IgG2^ did not change. The expression of CD23, but not I-A*", increased on the splenic B cells. IL-4 treatment did not affect the IL-4 production by Con A stimulated spleen cells, whereas it did decrease the IFN-7 production. In the same mice the TNP-specific IgGi and IgE serum levels, however, were decreased. Similar results were found when the antigen was continuously present during the IL-4 treatment. Furthermore, it was shown that IL-4 decreased the formation of IgGj and IgE memory cells. These results point to different effects of IL-4 in regulating antigen-specific and bystander responses.R. van Ommen.

show abstract

Section: Methodsmentioning

confidence: 99%

Prolonged In Vivo IL‐4 Treatment Inhibits Antigen‐Specific IgG1 and IgE Formation

1994

View full text Add to dashboard Cite

show abstract

“…For stimulation of BMMC via their Fc⑀R, MC were incubated with 5 g/ml IgE-anti-DNP Ab A2 (34, 35) for 48 -72 h. After washing, cross-linking was performed by 2.5 g/ml antiIgE mAb EM95.3 (36) in supplemented IMDM (10 6 cells per ml). Alternatively, BMMC were stimulated in the presence of 1 M ionomycin.…”

Section: Figurementioning

confidence: 99%

Specific and Redundant Roles for NFAT Transcription Factors in the Expression of Mast Cell-Derived Cytokines

Klein

Klein-Heßling

Palmetshofer

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

By virtue of their ability to express a plethora of biologically highly active mediators, mast cells (MC) are involved in both adaptive and innate immune responses. MC-derived Th2-type cytokines are thought to act as local amplifiers of Th2 reactions, including chronic inflammatory disorders such as allergic asthma, whereas MC-derived TNF-α is a critical initiator of antimicrobial defense. In this study, we demonstrate that the transcription factors NFATc1 and NFATc2 are part of a MC-specific signaling network that regulates the expression of TNF-α and IL-13, whereas NFATc3 is dispensable. Primary murine bone marrow-derived MC from NFATc2−/− mice, activated by either ionomycin or IgE/Ag cross-link, display a strong reduction in the production of these cytokines, compared with bone marrow-derived MC from wild-type mice. Detailed analyses of TNF-α and IL-13 expression using small interfering RNA-mediated knockdown reveals that both NFATc2 and NFATc1 are able to drive the expression of these cytokines, whereas neither degranulation nor the expression of IL-6 depends on NFAT activity. These results support the view that high NFAT activity is necessary for TNF-α and IL-13 promoter induction in MC, irrespective of whether NFATc2 or NFATc1 or a combination of both is present.

show abstract

“…Nonadherent cells were transferred to fresh culture plates every 2-3 days for a total of at least 21 days to remove adherent macrophages and fibroblasts. FACS analyses using an anti-CD13 Ab (R3-242, PharMingen, San Diego, CA) (32) and IgE plus anti-IgE mAb (33)(34)(35) as well as MayGrünwald-Giemsa and toluidine blue staining revealed that the resulting cell population consisted of Ͼ99% BMMC (data not shown).…”

Section: Generation Of Bmmcmentioning

confidence: 99%

IL-9 and IL-13 Production by Activated Mast Cells Is Strongly Enhanced in the Presence of Lipopolysaccharide: NF-κB Is Decisively Involved in the Expression of IL-9

Stassen

Müller

Arnold

et al. 2001

The Journal of Immunology

139

100

View full text Add to dashboard Cite

Mast cells, due to their ability to produce a large panel of mediators and cytokines, participate in a variety of processes in adaptive and innate immunity. Herein we report that in primary murine bone marrow-derived mast cells activated with ionomycin or IgE-Ag the bacterial endotoxin LPS strongly enhances the expression of IL-9 and IL-13, but not IL-4. This costimulatory effect of LPS is absent in activated mast cells derived from the LPS-hyporesponsive mouse strain BALB/c-LPSd, although in these cells the proinflammatory cytokine IL-1 can still substitute for LPS. The enhanced production of mast cell-derived IL-13 in the presence of IL-1 is a novel observation. Coactivation of mast cells with LPS leads to a synergistic activation of NF-κB, which is shown by an NF-κB-driven reporter gene construct. In the presence of an inhibitor of NF-κB activation, the production of IL-9 is strongly decreased, whereas the expression of IL-13 is hardly reduced, and that of IL-4 is not affected at all. NF-κB drives the expression of IL-9 via three NF-κB binding sites within the IL-9 promoter, which we characterize using gel shift analyses and reporter gene assays. In the light of recent reports that strongly support critical roles for IL-9 and IL-13 in allergic lung inflammation, our results emphasize the potential clinical importance of LPS as an enhancer of mast cell-derived IL-9 and IL-13 production in the course of inflammatory reactions and allergic diseases.

show abstract

Inhibition of IgE binding to mast cells and basophils by monoclonal antibodies to murine IgE

Cited by 126 publications

References 24 publications

Prolonged In Vivo IL‐4 Treatment Inhibits Antigen‐Specific IgG1 and IgE Formation

Prolonged In Vivo IL‐4 Treatment Inhibits Antigen‐Specific IgG1 and IgE Formation

Specific and Redundant Roles for NFAT Transcription Factors in the Expression of Mast Cell-Derived Cytokines

IL-9 and IL-13 Production by Activated Mast Cells Is Strongly Enhanced in the Presence of Lipopolysaccharide: NF-κB Is Decisively Involved in the Expression of IL-9

Contact Info

Product

Resources

About