Recognition of Species-Specific and Cross-Reacting Antigenic Determinants on House Dust Mite &lt;i&gt;(Dermatophagoides&lt;/i&gt;&lt;i&gt;)&lt;/i&gt; Allergens Using Monoclonal Antibodies

Hybridomas were produced after immunization with Der p I (Ag 42, P1). Specific anti-Der p I activity was detected in a reverse ELISA using immobilized anti-mouse Ig and highly purified Der p I labelled with horseradish peroxidase. Stable subclones from 6 parental hybridomas were obtained. The species specificities of the monoclonal antibodies (MABs) were classified: (1) by an overlayer technique analogous to the CRIE technique, and (2) by two competitive ELISA techniques. One MAB recognized an epitope specific for Dermatophagoides pteronyssinus. This MAB was successfully employed as a coating reagent in a species-specific ELISA for Der p I in house dust. The remaining antibodies reacted with epitopes shared to varying degrees by either of two other Dermatophagoides species. MABs recognizing epitopes common to all 3 species were not observed. Mutual cross-inhibition studies revealed four topographically distinct antibody binding sites on Der p I.

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Selection and Characterization of Monoclonal Antibodies against a Major Allergen in Dermatophagoidespteronyssinus

Horn¹,

Lind²

1987

“…Most mite-allergic patients show positive immedi ate skin tests to both D. pteronyssinus and D.farinae, suggesting that these species produce cross-reacting allergens [11,12). In fact, cross-reactivity has been ob served between antigen P, and Fr.l (major antigen of D. pteronyssinus and D.farinae, respectively) using monoclonal antibodies [13]. Marked cross-reactivity between D.farinae and D. pteronyssinus extracts was also observed in the present DTH system.…”

Section: Discussionmentioning

confidence: 99%

Strong Delayed-Type Hypersensitivity Induced against House Dust Mite Antigens in the Mice

Nakano

Yoshida²,

Shibata³

1989

The aim of this study was to assess the antigenicity of house dust mite antigens using delayed-type hypersensitivity (DTH) responses in mice. The crude extracts of Dermatophagoides pteronyssinus and Dermatophagoides farinae induced strong DTH reactions in mice when they were pretreated with cyclophosphamide. This reaction was typical of DTH responses and was transferred with T cells. Assessment of DTH responses to the house dust revealed that substantial cross-reactivity at T-cell level was observed between these two mite extracts. Almost all the fractions of the extract of D. pteronyssinus, which has a molecular weight of between 10 and 100 kilodaltons, elicited strong DTH responses. It was found that antigenicity of the mite extract was reduced by chemical denaturation with tannic acid.

“…The major house dust mite allergens Dcr p I and Der p 2 were puri fied from an extract of Dermatophagoides pteronyssinits by affinity chromatography using mAbs4Cl [19] and 6D6 [20], respectively. The major ragweed allergen Amb a I was purified from Ambrosia artemisiifolia pollen as described [21].…”

Section: Allergens Ami Antigensmentioning

confidence: 99%

Cytokine Priming of Human Basophils: Description of Allergen ‘Nonreleasers’

Black¹,

Lussier²,

Gion³

et al. 1996

Interleukins 3 and 5 and GM-CSF enhance histamine release from basophils triggered by various stimuli. In this report, we describe a subset of allergic patients whose basophils release histamine in response to allergen only when primed with cytokine. In the absence of cytokine, there is no detectable response to allergen. These patients, who represent 4–13% of the allergic population, cannot be distinguished by skin test reactivity or severity of allergic symptoms. Allergen nonreleasers tend to have lower titers of allergen-specific IgE than the majority of atopic subjects, but this difference is not significant (average titer of 29.8 for nonreleasers vs. 188 for typical allergies; p = 0.15). They release histamine normally with anti-IgE and with fMLP, indicating that basophils are responsive to signalling through the IgE receptor, and there is no intrinsic defect in degranulation. Thus, in these patients, the IgE-mediated release of inflammatory mediators from basophils is dependent on, rather than merely enhanced by, T cell cytokines. The relationship between these patients and the previously described anti-IgE ‘nonreleasers’ is discussed.