What is a mugwort allergy
Wolf M., T.E. Twaroch, S. Huber, M. Reithofer, M. Steiner, L. Aglas, M. Hauser, I. Aloisi, C. Asam, H. Hofer, M.A. Parigiani, C. Ebner, B. Bohle, P. Briza, A. Neubauer, F. Stolz, B. Jahn-Schmid, M. Wallner, F. Ferreira. Amb a 1 isoforms: unequal siblings with distinct immunological features.Allergy 72:1874-1882. (2017)
M. Reithofer and B.
Jahn-Schmid Review: Allergens with Protease Activity from Home Dust Mites. Int. J. Mol. Sci. 18: 1368. (2017)
Sancho A.I., M. Wallner, M. Hauser, B. Nagl, M. Himly, C.
Asam, C. Ebne, B. Jahn-Schmid, B. Bohle, F. Ferreira. T Cell Epitope-Containing Domains of Ragweed Amb a 1 and Mugwort Art v 6 Modulate Immunologic Responses in Humans and Mice. PLoS One 12(1):e0169784. (2017)
Selb, R., J. Eckl-Dorna, A. Neunkirchner, K. Schmetterer, K. Marth, J. Gamper, B. Jahn-Schmid, W. F. Pickl, R. Valenta, V. Niederberger. 2016. CD23 surface density on B cells is associated with IgE levels and determines IgE-facilitated allergen uptake as well as activation of allergen-specific T cells. J. Allergy Clin. Immunol.139: 290-299 (2017)
Rosskopf, S., S. Jutz, A.
Neunkirchner, M.R. Candia, B. Jahn-Schmid, B. Bohle, W.F. Pickl, P. Steinberger P. Creation of an engineered APC system to explore and optimize the presentation of immunodominant peptides of major allergens. Sci Rep. 6:31580. (2016)
B. Subbarayal , D. Schiller, C. Möbs, W. Pfützner, B. Jahn-Schmid, B. Gepp, H. Breiteneder, S. Vieths, B. Bohle The diversity of Bet v 1-specific IgG4 antibodies remains mostly constant during the course of birch pollen immunotherapy. J. Allergy Clin.
D. Van Hemelen, V. Mahler, G. Fischer, I. Fae, V. Reichl-Leb, W. Pickl, M. Jutel, S.
Smolinska, C. Ebner, B. Bohle, B. Jahn-Schmid. HLA class II peptide tetramers vs. allergen-induced proliferation for identification of allergen-specific CD4 T cells. Allergy 70:49-58 (2015)
S. Deifl, C. Zwicker, E. Vejvar, C.
Kitzmüller, G. Gadermaier, B. Nagl, S. Vrtala, P. Briza, G.J. Zlabinger, B.Jahn-Schmid, F. Ferreira, B. Bohle. Glutathione-S-transferase: a minor allergen in birch pollen due to limited release from hydrated pollen. PLoS One (2014)9(9):e109075.
S. Deifl, C. Kitzmüller, P. Steinberger, M. Himly, B. Jahn-Schmid, G. Fischer, G.J. Zlabinger, B. Bohle. Differential activation of dendritic cells by toll-like receptors causes diverse differentiation of naïve CD4+ T cells from allergic patients. Allergy.
69: 1602-9 (2014)
M. Geroldinger-Simic, T. Kinaciyan, B. Nagl., U. Baumgartner-Durchschlag, H. Huber, C. Ebner , J. Lidholm, D. Bartel, S. Vieths, B. Jahn-Schmid, B. Bohle. Oral exposure to Mal d 1 affects the immune response in patients with birch pollen allergy. J. Allergy Clin. Immunol. 131: 94-102 (2013) doi: 10.1016/j.jaci.2012.06.039.
Jahn-Schmid, B., M.
Hauser, N. Wopfner, P. Briza, U.E. Berger, R. Asero, C. Ebner, F. Ferreira, B. Bohle. Humoral and cellular cross-reactivity between Amb a 1, the major ragweed pollen allergen, and its mugwort homolog Art v 6.J. Immunol. 188: 1559-1567 (2012)
Knapp, B., GF. Fischer, D. Van Hemelen, I. Fae, B. Maillere, C. Ebner, W. Schreiner, B. Bohle, B. Jahn-Schmid. Association of HLA-DR1 with the allergic response to the major mugwort pollen allergen: molecular background.
BMC Immunology 13:43 (2012)
Kitzmüller, C., B. Nagl, S. Deifl, C. Walterskirchen, B. Jahn-Schmid, GJ. Zlabinger, B. Bohle. Human blood basophils do not act as antigen-presenting cells for the major birch pollen allergen Bet v 1.Allergy 67: 593-600 (2012)
Neunkirchner, A., V.M. Leb-Reichl, K.G. Schmetterer, S. Mutschlechner, H.J. Kueng D. Haiderer, K. Schuch, M. Wallner, B. Jahn-Schmid, B. Bohle, W. F. Pickl. Human TCR transgenic Bet v 1-specific Th1 cells suppress the effector function of Bet v 1-specific Th2 cells. J. Immunol. 187:4077-4087 (2011)
Reginald K, Westritschnig K, Linhart B, Focke-Tejkl M, Jahn-Schmid B,Eckl-Dorna J, Heratizadeh A, Stöcklinger A, Balic N, Spitzauer S, Niederberger V,Werfel T, Thalhamer J, Weidinger S, Novak N, Ollert M, Hirschl AM, Valenta R.Staphylococcus aureus fibronectin-binding protein specifically binds IgE from patients with atopic dermatitis and requires antigen presentation for cellularimmune responses.
J Allergy Clin Immunol.128(1):82-91.e8
Jahn-Schmid B, Pickl WF, Bohle B. Interaction of Allergens, Major Histocompatibility Complicated Molecules, and T Cell Receptors: A ‘Ménage à Trois’ That Opens New Avenues for Therapeutic Intervention in Type I Allergy. Int ArchAllergy Immunol.156(1):27-42.
Schulten V, Nagl B, Scala E, Bernardi ML, Mari A, Ciardiello MA, Lauer I,Scheurer S, Briza P, Jürets A, Ferreira F, Jahn-Schmid B, Fischer GF, Bohle B. Pru p 3, the nonspecific lipid transfer protein from peach, dominates the immuneresponse to its homolog in hazelnut.
Schmetterer KG, Haiderer D, Leb-Reichl VM, Neunkirchner A, Jahn-Schmid B, KüngHJ, Schuch K, Steinberger P, Bohle B, Pickl WF. Bet v 1-specific T-cell receptor/forkhead box protein 3 transgenic T cells suppress Bet v 1-specificT-cell effector function in an activation-dependent manner. J Allergy ClinImmunol.127(1):238-45.
RazzeraG, Gadermaier G, de Paula V, Almeida MS, Egger M, Jahn-Schmid B, Almeida FC, Ferreira F, Valente AP.
Mapping the interactions between a major pollen allergen and human IgE antibodies. Structure.18(8):1011-21.
Jahn-Schmid B, Wopfner N, Hubinger G, Asero R, Ebner C, Ferreira F, Bohle B.The T-cell response to Amb a 1 is characterized by 3 dominant epitopes and multiple MHC restriction elements. J Allergy Clin Immunol. 126(5):1068-71
Jahn-Schmid B. Allergy or tolerance, that’s the question. Int Arch AllergyImmunol. 152(3):195-6.
Gadermaier G, Jahn-Schmid B, Vogel L, Egger M, Himly M, Briza P, Ebner C,Vieths S, Bohle B, Ferreira F.
Targeting the cysteine-stabilized fold of Art v 1for immunotherapy of Artemisia pollen allergy. Mol Immunol.
Establishing a diagnosis of an allergy to mugwort
Defining the allergen responsible for eliciting signs and symptoms
-Responsible for allergic disease and/or anaphylactic episode
-To confirm sensitization prior to beginning immunotherapy
-To investigate the specificity of allergic reactions to insect venom allergens, drugs, or chemical allergens
Clinical manifestations of immediate hypersensitivity (allergic) diseases are caused by the release of proinflammatory mediators (histamine, leukotrienes, and prostaglandins) from immunoglobulin E (IgE)-sensitized effector cells (mast cells and basophils) when cell-bound IgE antibodies interact with allergen.
In vitro serum testing for IgE antibodies provides an indication of the immune response to allergen(s) that may be associated with allergic disease.
The allergens chosen for testing often depend upon the age of the patient, history of allergen exposure, season of the year, and clinical manifestations.
In individuals predisposed to develop allergic disease(s), the sequence of sensitization and clinical manifestations proceed as follows: eczema and respiratory disease (rhinitis and bronchospasm) in infants and children less than 5 years due to food sensitivity (milk, egg, soy, and wheat proteins) followed by respiratory disease (rhinitis and asthma) in older children and adults due to sensitivity to inhalant allergens (dust mite, mold, and pollen inhalants).
Detection of IgE antibodies in serum (Class 1 or greater) indicates an increased likelihood of allergic disease as opposed to other etiologies and defines the allergens that may be responsible for eliciting signs and symptoms.
The level of IgE antibodies in serum varies directly with the concentration of IgE antibodies expressed as a class score or kU/L.
Testing for IgE antibodies is not useful in patients previously treated with immunotherapy to determine if residual clinical sensitivity exists, or in patients in whom the medical management does not depend upon identification of allergen specificity.
Some individuals with clinically insignificant sensitivity to allergens may own measurable levels of IgE antibodies in serum, and results must be interpreted in the clinical context.
False-positive results for IgE antibodies may happen in patients with markedly elevated serum IgE (>2500 kU/L) due to nonspecific binding to allergen solid phases.
Homburger HA, Hamilton RG: Chapter 55: Allergic diseases.
In Henry’s Clinical Diagnosis and Management by Laboratory Methods.
23rd edition. Edited by RA McPherson, MR Pincus. Elsevier, 2017, pp 1057-1070