Interleukin 12 as an adjuvant to WI-1 adhesin immunization augments delayed-type hypersensitivity, shifts the subclass distribution of immunoglobulin G antibodies, and enhances protective immunity to Blastomyces dermatitidis infection

Cell-mediated immunity is pivotal in host resistance to Blastomyces dermatitidis infection. Immunization of mice with the WI-1 adhesin enhances resistance against experimental pulmonary infection but elicits features of a mixed T-helper-cell immune response. Immune mice acquire delayed-type hypersen...

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Bibliographic Details
Published in:Infection and immunity 2000-12, Vol.68 (12), p.7172-7174
Main Authors: WÜTHRICH, Marcel, FINKEL-JIMINEZ, Beatriz E, KLEIN, Bruce S
Format: Article
Language:English
Subjects:
adhesins
Adhesins, Bacterial - immunology
Adjuvants, Immunologic - pharmacology
Animals
Antibodies, Fungal - blood
Bacterial diseases
Bacteriology
Biological and medical sciences
Blastomyces - immunology
Blastomyces dermatitidis
Blastomycosis - prevention & control
Experimental bacterial diseases and models
Fundamental and applied biological sciences. Psychology
Fungal and Parasitic Infections
Hypersensitivity, Delayed - etiology
Immunization
Immunoglobulin G - classification
Infectious diseases
Interleukin-12 - pharmacology
Medical sciences
Mice
Microbiology
Vaccines, antisera, therapeutical immunoglobulins and monoclonal antibodies
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Summary:Cell-mediated immunity is pivotal in host resistance to Blastomyces dermatitidis infection. Immunization of mice with the WI-1 adhesin enhances resistance against experimental pulmonary infection but elicits features of a mixed T-helper-cell immune response. Immune mice acquire delayed-type hypersensitivity (DTH) but also high titers of WI-1-specific immunoglobulin G1 (IgG1) and IgG2b, a result indicative of T-helper-2 cellular immunity. We report that interleukin-12, used as an adjuvant for WI-1 immunization, augments DTH, shifts the balance of the T-helper phenotype toward Th1, and enhances resistance to B. dermatitidis infection.
ISSN:0019-9567
1098-5522
DOI:10.1128/IAI.68.12.7172-7174.2000