Inhibition of Human Lung Mast Cell Sensitization by IgE in Allergic Sera

Coleman, John W.; Godfrey, Richard

doi:10.1159/000232855

Cited by 6 publications

(6 citation statements)

References 5 publications

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“…These results are in agreement with previ ous reports where rats actively synthesizing IgE anti body or bearing IgE myeloma tumors were unable to be passively sensitized [7,8], IgE present in sera of parasitized individuals or IgE against another specif icity could effectively block sensitization of human lung mast cells if added before pollen-specific IgE, but was less effective if presented to mast cells simul taneously with reaginic sera and ineffective if added after sensitization [2,3].…”

Section: Discussionsupporting

confidence: 91%

“…Passive sensitization of mast cells in hu man chopped-lung fragments was inhibited by treat ment with IgE-rich sera from parasitized individuals or by IgE of other specificities [2,3]. Myeloma IgE (mlgE) or its Fc fragment blocked the PrausnitzKustner reaction in a healthy person when adminis tered 24 h prior to or simultaneously with antigenspecific IgE [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of Anaphylactic Histamine Release and Pulmonary Distress in Rats by Nonspecific IgE

Butchko¹,

Aspinall²,

Smith³

1984

Int Arch Allergy Immunol

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Myeloma IgE, obtained from ascitic fluid of rats previously inoculated with the IgE-producing cell line IR-162, was administered in prophylactic and therapeutic regimens to rats passively and actively sensitized to ovalbumin. Administration of myeloma IgE prior to passive sensitization resulted in ∼95% inhibition of anaphylactic histamine release and significant protection from anaphylactic pulmonary distress. Myeloma IgE treatment prior and subsequent to active sensitization brought about a 70–80% inhibition of anaphylactic histamine release. A similar pattern of protection was seen in animals that received 5 but not 3 weekly myeloma IgE treatments subsequent to active sensitization. These findings indicate that treatment with nonspecific IgE prior to sensitization is effective in blocking anaphylactic reactions but competition with cell-bound IgE in sensitized animals requires prolonged administration of relatively large quantities of ‘nonsense’ IgE.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Inhibition of Anaphylactic Histamine Release and Pulmonary Distress in Rats by Nonspecific IgE

Butchko¹,

Aspinall²,

Smith³

1984

Int Arch Allergy Immunol

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“…Similar patterns of IgE production have been reported previously in serum [30, 31] and at a cellular level [32, 33] in the BN rat. Non‐specific IgE has been shown to block the responsiveness of mast cells to specific antigen challenge [9, 10, 34]. In the present study however, despite the low ratio of OVA‐specific to total IgE secreting cells, serum from days 10 and 15 was still able to efficiently arm RBL cells.…”

Section: Discussioncontrasting

confidence: 55%

“…While this has proven to be clinically useful, the predictive potential of serum IgE concentrations is far from perfect [6]. Other influences such as nonspecific IgE, which is a feature of allergic disease [7] and of helminth infection [8], may also be important in determining mast‐cell reactivity [9, 10]. In contrast, high affinity may be relatively unimportant for IgE function [11].…”

Section: Introductionmentioning

confidence: 99%

The Biological Activity of Serum IgE Changes over the Course of a Primary Response

2002

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Mast-cell degranulation is triggered by the bridging of Fc receptor-bound antigen-specific immunoglobulin IgE on the cell surface. In vitro experiments suggest that antibody affinity and nonspecific IgE may affect the mast-cell function, however, their importance in vivo is unclear. Investigations of the effects of these parameters on mast-cell sensitization were therefore carried out in a rat immunization model in which the IgE response is transient and peaks on days 10±15. Between these two timepoints, significant changes in the level of specific IgE were not observed, but the avidity of specific IgE increased (P < 0.05). Total serum IgE peaked on day 10 and slowly declined, with the relative proportion of specific to total IgE increasing from day 10±15 (P < 0.05). Despite similar levels of antigen-specific IgE, increasing avidity and an increased proportion of specific IgE between days 10 and 15, the biological activity of IgE in the serum peaks on day 10 and declines rapidly, dropping around seven-fold by day 15 (P < 0.001). Mechanisms that could explain this finding, such as differential expression of IgE isoforms and changes in the fine specificity of the IgE response, are discussed.

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“…The second factor that could possibly bear relation to the low cutaneous reactivity ofthe LSEL is reflected by the depressed positivity of P-K tests in this group. Various studies have suggested that the high levels of polyclonal IgE induced by parasitic infection may competitively inhibit the capacity of IgE antibody ofa given specificity to sensitize the target cells [17,[26][27][28][29][30]. We showed that the cutaneous sensitivity ofthe LSEL to histamine was not altered, and that the basic integrity ofthe mast cells was maintained, as judged by reactivity to codeine and anti-IgE.…”

Section: Discussionmentioning

confidence: 73%

Allergic reactivity and socio‐economic level in a tropical environment

Lynch

López

Prisco-Fuenmayor

et al. 1987

Clin Experimental Allergy

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As some factors associated with the tropical environment can modify the expression of atopie disease, various indicators of allergic reactivity were compared between allergic and non-allergic subjects of different socio-economic level in Caracas, Venezuela (Lat. 10°N). The socio-economic levels considered were high (HSEL), medium-high (MSEL) or low (LSEL). As generally found in temperature climates, in the HSEL the total serum IgE levels of allergic patients were significantly greater than those of nonallergic individuals (geometric means of 274 vs 126 IU/ml, respectively), as were also the specific serum IgE antibody levels (55-6 vs 23-8% positive, respectively, for house dust). These results correlated closely with the skin-test reactivity of these subjects (60-3 vs 17-5% positive for house dust). In this group, the degree of intestinal helminthic infection was low (5-6% positive for Ascaris). In contrast, for the MSEL where the degree of parasitic infection was higher (13-0%), the total serum IgE levels were elevated in both allergic and non-allergic subjects (602 vs 363 IU/ml). Similarly, positivity for specific IgE antibody was high, and comparable between allergies and non-allergies of this group (61-5 vs 54-2%), as was also the case for skin-test reactivity (71-9 vs 60-4%). In the LSEL, parasitic infection was prevalent (47-6%), and the total serum IgE levels were markedly elevated, with little difference occurring between allergic and non-allergic individuals (2269 vs 1981 IU/ml). The positivity for specific IgE antibody was high, and effectively independent of the allergic state (75-6 vs 53-7%), but in contrast the skin test reactivity was relatively low (22-0 vs 9-8%). The lack of correlation between skin test and specific IgE results in this group appeared to have Correspondence: Dr Neil R. Lynch, Instituto de Biomedicina, Aptdo. 4043, Caracas lOlOA, Venezuela. N. R. Lynch et al. two causes. Firstly, although the frequency of positivity in specific IgE was high, only low grade antibody activity was detected. Secondly, studies ofskin reactivity indicated that some form of interference to target cell sensitization was occurring. The possible participation of helminth-induced polyclonally-increased IgE synthesis in the modification of allergic reactivity is discussed.

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Inhibition of Human Lung Mast Cell Sensitization by IgE in Allergic Sera

Cited by 6 publications

References 5 publications

Inhibition of Anaphylactic Histamine Release and Pulmonary Distress in Rats by Nonspecific IgE

Inhibition of Anaphylactic Histamine Release and Pulmonary Distress in Rats by Nonspecific IgE

The Biological Activity of Serum IgE Changes over the Course of a Primary Response

Allergic reactivity and socio‐economic level in a tropical environment

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