http://www.clinicalmolecularallergy.com The most accessed research articles published by Clinical and Molecular Allergy 2012-04-23T00:00:00Z Dysregulated immune response results in inflammatory symptoms in the respiratory mucosa leading to asthma and allergy in susceptible individuals. The T helper type 2 (Th2) subsets are primarily involved in this disease process. Nevertheless, there is growing evidence in support of T cells with regulatory potential that operates in non-allergic individuals. These regulatory T cells occur naturally are called natural T regulatory cells (nTregs) and express the transcription factor Foxp3. They are selected in the thymus and move to the periphery. The CD4 Th cells in the periphery can be induced to become regulatory T cells and hence called induced or adaptive T regulatory cells. These cells can make IL-10 or TGF-b or both, by which they attain most of their suppressive activity. This review gives an overview of the regulatory T cells, their role in allergic diseases and explores possible interventionist approaches to manipulate Tregs for achieving therapeutic goals. http://www.clinicalmolecularallergy.com/content/7/1/5 Subhadra Nandakumar Christopher Miller Uday Kumaraguru Clinical and Molecular Allergy 2009, null:5 2009-03-12T00:00:00Z doi:10.1186/1476-7961-7-5 /content/figures/1476-7961-7-5-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 5 2009-03-12T00:00:00Z XML In Asian countries where the Buddhism and Taoism are mainstream religions, incense burning is a daily practice. A typical composition of stick incense consists of 21% (by weight) of herbal and wood powder, 35% of fragrance material, 11% of adhesive powder, and 33% of bamboo stick. Incense smoke (fumes) contains particulate matter (PM), gas products and many organic compounds. On average, incense burning produces particulates greater than 45 mg/g burned as compared to 10 mg/g burned for cigarettes. The gas products from burning incense include CO, CO2, NO2, SO2, and others. Incense burning also produces volatile organic compounds, such as benzene, toluene, and xylenes, as well as aldehydes and polycyclic aromatic hydrocarbons (PAHs). The air pollution in and around various temples has been documented to have harmful effects on health. When incense smoke pollutants are inhaled, they cause respiratory system dysfunction. Incense smoke is a risk factor for elevated cord blood IgE levels and has been indicated to cause allergic contact dermatitis. Incense smoke also has been associated with neoplasm and extracts of particulate matter from incense smoke are found to be mutagenic in the Ames Salmonella test with TA98 and activation. In order to prevent airway disease and other health problem, it is advisable that people should reduce the exposure time when they worship at the temple with heavy incense smokes, and ventilate their house when they burn incense at home. http://www.clinicalmolecularallergy.com/content/6/1/3 Ta-Chang Lin Guha Krishnaswamy David Chi Clinical and Molecular Allergy 2008, null:3 2008-04-25T00:00:00Z doi:10.1186/1476-7961-6-3 Health risks posed by incense smoke Incense burning in Buddhist and Taoist temples is regular practice, however inhalation of incense gas products can cause respiratory disease and other health problems, so worshippers are advised to reduce exposure times, and ventilate their houses when they burn incense at home. /content/figures/1476-7961-6-3-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 3 2008-04-25T00:00:00Z XML Autoimmune progesterone dermatitis (APD) is a condition in which the menstrual cycle is associated with a number of skin findings such as urticaria, eczema, angioedema, and others. In affected women, it occurs 3–10 days prior to the onset of menstrual flow, and resolves 2 days into menses. Women with irregular menses may not have this clear correlation, and therefore may be missed. We present a case of APD in a woman with irregular menses and urticaria/angioedema for over 20 years, who had not been diagnosed or correctly treated due to the variable timing of skin manifestations and menses. In addition, we review the medical literature in regards to clinical features, pathogenesis, diagnosis, and treatment options. http://www.clinicalmolecularallergy.com/content/2/1/10 Alan Baptist James Baldwin Clinical and Molecular Allergy 2004, null:10 2004-08-02T00:00:00Z doi:10.1186/1476-7961-2-10 /content/figures/1476-7961-2-10-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 10 2004-08-02T00:00:00Z XML Tinea pedis is a chronic fungal infection of the feet, very often observed in patients who are immuno-suppressed or have diabetes mellitus. The practicing allergist may be called upon to treat this disease for various reasons. Sometimes tinea infection may be mistaken for atopic dermatitis or allergic eczema. In other patients, tinea pedis may complicate allergy and asthma and may contribute to refractory atopic disease. Patients with recurrent cellulitis may be referred to the allergist/immunologist for an immune evaluation and discovered to have tinea pedis as a predisposing factor. From a molecular standpoint, superficial fungal infections may induce a type2 T helper cell response (Th2) that can aggravate atopy. Th2 cytokines may induce eosinophil recruitment and immunoglobulin E (IgE) class switching by B cells, thereby leading to exacerbation of atopic conditions. Three groups of fungal pathogens, referred to as dermatophytes, have been shown to cause tinea pedis: Trychophyton sp, Epidermophyton sp, and Microsporum sp. The disease manifests as a pruritic, erythematous, scaly eruption on the foot and depending on its location, three variants have been described: interdigital type, moccasin type, and vesiculobullous type. Tinea pedis may be associated with recurrent cellulitis, as the fungal pathogens provide a portal for bacterial invasion of subcutaneous tissues. In some cases of refractory asthma, treatment of the associated tinea pedis infection may induce remission in airway disease. Very often, protracted topical and/or oral antifungal agents are required to treat this often frustrating and morbid disease. An evaluation for underlying immuno-suppression or diabetes may be indicated in patients with refractory disease. http://www.clinicalmolecularallergy.com/content/2/1/5 Muhannad Al Hasan S. Matthew Fitzgerald Mahnaz Saoudian Guha Krishnaswamy Clinical and Molecular Allergy 2004, null:5 2004-03-29T00:00:00Z doi:10.1186/1476-7961-2-5 /content/figures/1476-7961-2-5-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 5 2004-03-29T00:00:00Z XML Background: Major histocompatibility complex class II deficiency, also referred to as bare lymphocyte syndrome is a rare primary Immunodeficiency disorder characterized by a profondly deficient human leukocyte antigen class II expression and a lack of cellular and humoral immune responses to foreign antigens. Clinical manifestations include extreme susceptibility to viral, bacterial, and fungal infections. The infections begin in the first year of life and involve usually the respiratory system and the gastrointestinal tract. Severe malabsorption with failure to thrive ensues, often leading to death in early childhood. Bone marrow transplantation is the curative treatment.Case reportsHere we report two cases with a late outcome MHC class II deficiency. They had a long term history of recurrent bronchopulmonary and gastrointestinal infections. Bone marrow transplantation could not be performed because no compatible donor had been identified. At the age of 12 years, they developed oral papillomatous lesions related to HPV (human papillomavirus). The diagnosis of HPV infection was done by histological examination. HPV typing performed on the tissue obtained at biopsy showed HPV type 6. The lesions were partially removed after two months of laser treatment. Conclusions: Viral infections are common in patients with MHC class II and remain the main cause of death. Besides warts caused by HPV infection do not exhibit a propensity for malignant transformation; they can cause great psychosocial morbidity. http://www.clinicalmolecularallergy.com/content/10/1/6 Naouel Guirat-Dhouib Yemen Baccar Imene Ben Mustapha Monia Ouederni Sameh Chouaibi Nadia ElFekih Mohamed Ridha Barbouche Bassima Fezaa Ridha Kouki Slama Hmida Fethi Mellouli Mohamed Bejaoui Clinical and Molecular Allergy 2012, null:6 2012-04-23T00:00:00Z doi:10.1186/1476-7961-10-6 /content/figures/1476-7961-10-6-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 6 2012-04-23T00:00:00Z XML The diagnosis of immediate allergy is mainly based upon an evocative clinical history, positive skin tests (gold standard) and, if available, detection of specific IgE. In some complicated cases, functional in vitro tests are necessary. The general concept of those tests is to mimic in vitro the contact between allergens and circulating basophils. The first approach to basophil functional responses was the histamine release test but this has remained controversial due to insufficient sensitivity and specificity. During recent years an increasing number of studies have demonstrated that flow cytometry is a reliable tool for monitoring basophil activation upon allergen challenge by detecting surface expression of degranulation/activation markers (CD63 or CD203c). This article reviews the recent improvements to the basophil activation test made possible by flow cytometry, focusing on the use of anti-CRTH2/DP2 antibodies for basophil recognition. On the basis of a new triple staining protocol, the basophil activation test has become a standardized tool for in vitro diagnosis of immediate allergy. It is also suitable for pharmacological studies on non-purified human basophils. Multicenter studies are now required for its clinical assessment in large patient populations and to define the cut-off values for clinical decision-making. http://www.clinicalmolecularallergy.com/content/3/1/9 Radhia Boumiza Anne-lise Debard Guillaume Monneret Clinical and Molecular Allergy 2005, null:9 2005-06-30T00:00:00Z doi:10.1186/1476-7961-3-9 /content/figures/1476-7961-3-9-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 9 2005-06-30T00:00:00Z XML Asthma belongs to the category of classical allergic diseases which generally arise due to IgE mediated hypersensitivity to environmental triggers. Since its prevalence is very high in developed or urbanized societies it is also referred to as "disease of civilizations". Due to its increased prevalence among related individuals, it was understood quite long back that it is a genetic disorder. Well designed epidemiological studies reinforced these views. The advent of modern biological technology saw further refinements in our understanding of genetics of asthma and led to the realization that asthma is not a disorder with simple Mendelian mode of inheritance but a multifactorial disorder of the airways brought about by complex interaction between genetic and environmental factors. Current asthma research has witnessed evidences that are compelling researchers to redefine asthma altogether. Although no consensus exists among workers regarding its definition, it seems obvious that several pathologies, all affecting the airways, have been clubbed into one common category called asthma. Needless to say, genetic studies have led from the front in bringing about these transformations. Genomics, molecular biology, immunology and other interrelated disciplines have unearthed data that has changed the way we think about asthma now. In this review, we center our discussions on genetic basis of asthma; the molecular mechanisms involved in its pathogenesis. Taking cue from the existing data we would briefly ponder over the future directions that should improve our understanding of asthma pathogenesis. http://www.clinicalmolecularallergy.com/content/7/1/7 Amrendra Kumar Balaram Ghosh Clinical and Molecular Allergy 2009, null:7 2009-05-06T00:00:00Z doi:10.1186/1476-7961-7-7 /content/figures/1476-7961-7-7-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 7 2009-05-06T00:00:00Z XML ObjectiveWhile most allergic responses to food are directed against protein epitopes and occur within 30 minutes of ingesting the allergen, recent studies suggest that delayed reactions may occur, sometimes mediated by IgE antibodies directed against carbohydrate moieties. The objective of this review is to summarize the clinical features and management of delayed hypersensitivity reactions to mammalian meat mediated by IgE antibodies to galactose-alpha 1,3-galactose (alpha-gal), an oligosaccharide. Methods: A PubMed search was conducted with MeSH terms: galactosyl-(1,3) galactose, oligosaccharides, cetuximab, allergy/hypersensitivity, and anaphylaxis. Reported cases with alpha-gal-mediated reactions were reviewed. This research study was approved by the Institutional Review Board of East Tennessee State University. Results: Thirty-two cases of adults presenting with red-meat induced allergy thought to be related to oligosaccharides have been reported in the literature so far, making this a rare and evolving syndrome. Most of these patients demonstrated delayed reactions to beef, as was seen in the case reported by us in this manuscript. IgE specific to alpha-gal was identified in most patients with variable response to skin testing with beef and pork. Inhibition studies in some cases showed that the IgE antibodies to beef were directed towards alpha-gal in the meat rather than the protein. The patients often reported history of tick bites, the significance of which is unclear at present. Reactions to cetuximab, a monoclonal antibody, are mediated by a similar mechanism, with IgE antibodies directed against an alpha-gal moiety incorporated in the drug structure. Conclusion: Alpha-gal is an oligosaccharide recently incriminated in delayed anaphylactic reactions to mammalian meats such as to beef, pork, and lamb. It appears that anaphylactic reactions to the anti-cancer biological agent, cetuximab, may be linked mechanistically to the same process. More studies are required to understand the underlying molecular basis for these delayed reactions in specific, and their broader implications for host defense in general. http://www.clinicalmolecularallergy.com/content/10/1/5 Hana Saleh Scott Embry Andromeda Nauli Seif Atyia Guha Krishnaswamy Clinical and Molecular Allergy 2012, null:5 2012-03-07T00:00:00Z doi:10.1186/1476-7961-10-5 /content/figures/1476-7961-10-5-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 5 2012-03-07T00:00:00Z PDF Background: Cow's milk allergy is one of the most common food allergies among younger children. We investigated IgE antibodies to milk, and IgE and IgG4 antibodies to casein, α-lactalbumin and β-lactoglobulin in cow's milk allergic (CMA) and non-allergic (non-CMA) children in order to study their clinical usefulness. Methods: Eighty-three children with suspected milk allergy (median age: 3.5 years, range: 0.8-15.8 years) were diagnosed as CMA (n = 61) or non-CMA (n = 22) based on an open milk challenge or convincing clinical history. Their serum concentrations of allergen-specific (s) IgE and IgG4 antibodies were measured using ImmunoCAP®. For the sIgG4 analysis, 28 atopic and 31 non-atopic control children were additionally included (all non-milk sensitized). Results: The CMA group had significantly higher levels of milk-, casein- and β-lactoglobulin-sIgE antibodies as compared to the non-CMA group. The casein test showed the best discriminating performance with a clinical decision point of 6.6 kUA/L corresponding to 100% specificity. All but one of the CMA children aged > 5 years had casein-sIgE levels > 6.6 kUA/L. The non-CMA group had significantly higher sIgG4 levels against all three milk allergens compared to the CMA group. This was most pronounced for casein-sIgG4 in non-CMA children without history of previous milk allergy. These children had significantly higher casein-sIgG4 levels compared to any other group, including the non-milk sensitized control children. Conclusions: High levels of casein-sIgE antibodies are strongly associated with milk allergy in children and might be associated with prolonged allergy. Elevated casein-sIgG4 levels in milk-sensitized individuals on normal diet indicate a modified Th2 response. However, the protective role of IgG4 antibodies in milk allergy is unclear. http://www.clinicalmolecularallergy.com/content/10/1/1 Komei Ito Masaki Futamura Robert Moverare Akira Tanaka Tsutomu Kawabe Tatsuo Sakamoto Magnus Borres Clinical and Molecular Allergy 2012, null:1 2012-01-02T00:00:00Z doi:10.1186/1476-7961-10-1 /content/figures/1476-7961-10-1-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 1 2012-01-02T00:00:00Z XML Background: In 2006, the Norwegian Medicines Agency mandated a switch from desloratadine, ebastine, or fexofenadine to cetirizine or loratadine in patients with allergic rhinitis (AR) or chronic urticaria (CU). In an online survey, patients whose medication was switched assessed the impact on efficacy, fatigue, and work productivity/attendance. Methods: Allergy patients in Norway completed a 25-item online survey. Patients aged ≥ 18 years with AR or CU who were switched to cetirizine or loratadine from desloratadine, ebastine, or fexofenadine were included. Participants rated post-switch efficacy, fatigue, and effect on work productivity/attendance compared with their pre-switch medication. Patients also reported post-switch change in number of doctor visits required, total treatment cost, and whether they had switched or wanted to switch back to their previous medications. Results: Of 1920 patients invited, 493 responded and 409 of these were eligible. Previous antihistamines were desloratadine (78.4% of respondents), ebastine (16.0%), and fexofenadine (5.6%). Post-switch, 64.7% received cetirizine and 35.3% loratadine. Compared with previous therapy, cetirizine and loratadine were rated less effective by 46.3% of respondents; 28.7% reported increased fatigue; and 31.6% reported decreased work productivity with the generic agents. At the time of the survey, 26% of respondents had switched back to their previous medication. Conclusions: This is the first survey to assess the impact on patient-reported outcomes of a mandated switch from prescription to generic antihistamines in Norway. The findings suggest that patient response to different antihistamines will vary and that treatment decisions should be individualized for optimal results. http://www.clinicalmolecularallergy.com/content/9/1/5 Fredrik Thorn Halvor Celius Tone Odegard Randeep Mandla Erik Hexeberg Clinical and Molecular Allergy 2011, null:5 2011-02-28T00:00:00Z doi:10.1186/1476-7961-9-5 /content/figures/1476-7961-9-5-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 5 2011-02-28T00:00:00Z XML