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Production of a recombinant version of a Heligmosomoides polygyrus antigen that is preferentially recognized by resistant mouse strains
Author(s) -
Hoselton Scott,
Piche Lisa,
Gustad Thomas,
Robinson Michael
Publication year - 2002
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1046/j.1365-3024.2002.00483.x
Subject(s) - heligmosomoides polygyrus , biology , antigen , immune system , antibody , immunology , recombinant dna , immunity , monoclonal antibody , immunization , virology , microbiology and biotechnology , genetics , gene
Summary Protective immunity to the mouse nematode parasite, Heligmosomoides polygyrus, has been characterized and found to be composed of the Th2 type. However, many inbred mouse strains cannot produce this protective immune response during a primary infection. A possible reason for this lack of protection in poor responding strains could be due to lack of recognition of specific protective antigens by these strains. Recently, evidence suggests that specific antigens exist that are only recognized by fast responding strains during a primary infection. Using monoclonal antibodies to screen an H. polygyrus cDNA library enabled the production of a recombinant protein, 3A4, which is antigenically similar to those found in the excretory/secretory antigens (E/S) of both L4 and adult parasites. Protein 3A4 shares approximately 70% sequence homology with an E/S protein that induces protection to Trichostrongylus colubriformis in guinea‐pigs. Antibodies that bind to 3A4 are preferentially produced in SWR compared to BALB/c mice following immunization with L4 homogenate, although both strains of mice were able to produce comparable levels of specific antibodies after immunization with 3A4 protein. It is believed that 3A4 may have considerable importance in dissecting out the nature of the immune response to H. polygyrus infection, particularly in mouse strains of differing response phenotype.