Coprinus comatus (shaggy cap) is a potential source of aeroallergen that may provoke atopic dermatitis

Fischer, Barbra; Yawalkar, Nikhil; Brander, Karl A.; Pichler, Werner J.; Helbling, Arthur

doi:10.1016/s0091-6749(99)70295-2

Cited by 22 publications

(14 citation statements)

References 29 publications

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“…A relationship between circulating specific T cells (Th2 profile) and positive APT reactions to M. furfur has been discussed [45]. Another allergen recently described to elicit positive APT reactions derives from shaggy cap (Coprinus comatus), an edible mushroom of the Basidiomycetes family [46].…”

Section: Correlation Of Atopy Patch Test Results To Clinical Featuresmentioning

confidence: 99%

Lessons from atopy patch testing in Atopic Dermatitis

Kerschenlohr

Darsow

Burgdorf

et al. 2004

Curr Allergy Asthma Rep

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The exposure of atopic eczema (AE) patients to their relevant protein allergens (eg, from house dust mite, cat dander, grass pollen, or food allergens) can trigger an exacerbation or maintain the disease. Diagnostic procedures are needed to specify allergen avoidance recommendations for the individual patient. Skin prick tests and specific serum IgE tests might be helpful in pointing out potential trigger factors, but relevance needs to be confirmed (eg, with food provocation tests). The atopy patch test (APT) involves the epicutaneous application of intact protein allergens in a diagnostic patch test setting with an evaluation of the induced eczematous skin lesions after 24 to 72 hours. The APT targets the cellular component of AE and helps round out the AE test spectrum. As a number of apparently minor test modifications greatly influence the sensitivity, specificity, and reproducibility of the APT, the European Task Force on Atopic Dermatitis (ETFAD) has developed a standardized APT technique. It consists of purified allergen preparations in petrolatum, applied in 12-mm diameter Finn chambers mounted on Scanpor tape to non-irritated, non-abraded, or tape-stripped skin of the upper back. The APT is read at 48 and 72 hours according to the test criteria and reading key of the ETFAD for appearance of erythema, and number and distribution pattern of the papules. In contrast with skin prick tests, the APT might even detect a relevant sensitization in the absence of specific IgE. Many studies have been undertaken to objectify the sensitivity and specificity of the APT to show its diagnostic use in clinical practice.

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Section: Correlation Of Atopy Patch Test Results To Clinical Featuresmentioning

confidence: 99%

Lessons from atopy patch testing in Atopic Dermatitis

Kerschenlohr

Darsow

Burgdorf

et al. 2004

Curr Allergy Asthma Rep

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“…For example, sensitization may exist for airborne fungal antigens derived from the Coprinus comatus. 42 Other explanations can be that a subset of type 2 T cells incapable of producing interleukin 4 may be active and thus not stimulating IgE production 43 or that IgE antibodies are only present on dendritic cells 44,45 or that the allergen-directed inflammatory response has slowly evolved into autoantigen-directed chronic immune reactions. 46,47 In conclusion, if one accepts allergen-specific IgE to be essential for the diagnosis of AD, AFD should be regarded as an entity distinct from AD with several specific characteristics.…”

Section: Discussionmentioning

confidence: 99%

Clinical differences between atopic and atopiform dermatitis

Brenninkmeijer

Spuls

Legierse

et al. 2008

Journal of the American Academy of Dermatology

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“…Many factors may be involved in the development of AD, including the presence of specific genes within the individual's genetic material (147); exposure to various environmental (144,443), food (448), or microbial (2) allergens; and immunological disturbances within the skin. The pivotal role of the immune system is demonstrated by the acquisition of AD by a previously nonatopic individual after a bone marrow transplant (6).…”

Section: Atopic Dermatitismentioning

confidence: 99%

Immunology of Diseases Associated withMalasseziaSpecies

2002

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SUMMARY Malassezia species are members of the human cutaneous commensal flora, in addition to causing a wide range of cutaneous and systemic diseases in suitably predisposed individuals. Studies examining cellular and humoral immune responses specific to Malassezia species in patients with Malassezia-associated diseases and healthy controls have generally been unable to define significant differences in their immune response. The use of varied antigenic preparations and strains from different Malassezia classifications may partly be responsible for this, although these problems can now be overcome by using techniques based on recent work defining some important antigens and also a new taxonomy for the genus. The finding that the genus Malassezia is immunomodulatory is important in understanding its ability to cause disease. Stimulation of the reticuloendothelial system and activation of the complement cascade contrasts with its ability to suppress cytokine release and downregulate phagocytic uptake and killing. The lipid-rich layer around the yeast appears to be pivotal in this alteration of phenotype. Defining the nonspecific immune response to Malassezia species and the way in which the organisms modulate it may well be the key to understanding how Malassezia species can exist as both commensals and pathogens.

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Coprinus comatus (shaggy cap) is a potential source of aeroallergen that may provoke atopic dermatitis

Cited by 22 publications

References 29 publications

Lessons from atopy patch testing in Atopic Dermatitis

Lessons from atopy patch testing in Atopic Dermatitis

Clinical differences between atopic and atopiform dermatitis

Immunology of Diseases Associated withMalasseziaSpecies

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