IMMUNE RESPONSE TO N-TERMINAL AND C-TERMINAL DELETION MUTANTS OF ASPERGILLUS FUMIGATUS MAJOR ALLERGEN ASP F 3
Journal Title: Indian Journal of Clinical Biochemistry - Year 2006, Vol 21, Issue 2
Abstract
20 ABSTRACT The ubiquitous fungus Aspergillus fumigatus causes allergic rhinitis, asthma, sinusitis and allergic bronchopulmonary aspergillosis. A number of major allergens from A. fumigatus are purified, but their structurefunction role in the pathogenesis of disease is not known. Such information is essential for devising alternative therapy of fungal allergic diseases. In the present study, N-terminal and C-terminal deletion mutants of Asp f 3 were constructed and their immunopathological responses studied in a mice model of allergy. Three mutants viz, Asp f 3 (aa 33-168), (aa 1-142), and (aa 23-142) were made by deleting certain amino acids from epitopic regions of full length Asp f 3, a major allergen of A. fumigatus. The Asp f 3 and three mutated proteins were expressed in pET vector. The C-terminal deletion mutant Asp f 3 (aa 1-142) induced elevated IFN- γ but low levels of IL-4 by spleen cells. This mutant also showed significant downregulation of peripheral blood eosinophils and lung inflammation in immunized mice. The N-terminal deletion mutant Asp f 3 (aa 33-168) also exhibited an immuno-suppressive effect in terms of IgE production and induction of Th2 cytokine. The results indicate that rAsp f 3 and its deletion mutants induced distinct immune-inflammatory responses in mice on challenge with these proteins. The non-IgE binding deletion mutants of Asp f 3 (aa 1-142 and aa 33-168) could deviate Th2 immune response with a concomitant reduction in airway inflammation and infiltration of inflammatory cells. KEY WORDS Aspergillus fumigatus, rAsp f 3, Deletion mutants, Murine model, ABPA Address for Correspondence: Dr. B.P. Singh Scientist F, Allergy and Immunology Section Institute of Genomics and Integrative Biology Delhi University Campus Mall Road, Delhi-110007 INDIA E- INTRODUCTION Aspergillus fumigatus (Af), is responsible for a wide range of allergic diseases in humans such as allergic rhinitis, fungal sinusitis, asthma, and allergic bronchopulmonary aspergillosis (1). Studies in both humans and mice models demonstrated that these diseases are characterized predominantly by a Th2 response (2). The protective immune response to Af is mostly due to a CD4+ Th1 lymphocyte response. The involvement of Af-specific Th1 cytokines in allergic response raise the possibility of uncovering effective therapeutic modalities that
Authors and Affiliations
*Bhanu Singh, Banani Banerjee,, Puspanita Naik,, Jordan Fink, Viswanath Kurup
Keywords
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