The adjuvanticity of gamma inulin.
Identifieur interne : 002E49 ( Main/Exploration ); précédent : 002E48; suivant : 002E50The adjuvanticity of gamma inulin.
Auteurs : P D Cooper ; E J SteeleSource :
- Immunology and cell biology [ 0818-9641 ]
Descripteurs français
- KwdFr :
- MESH :
- biosynthèse : Immunoglobulines.
- immunologie : Lymphocytes T cytotoxiques, Orthomyxoviridae.
- pharmacologie : Inuline.
- Adjuvants immunologiques, Animaux, Femelle, Hypersensibilité retardée, Lignées consanguines de souris, Souris, Voie alterne d'activation du complément.
English descriptors
- KwdEn :
- MESH :
- chemical , biosynthesis : Immunoglobulins.
- chemical , immunology : Hemocyanins.
- chemical , pharmacology : Inulin.
- chemical : Adjuvants, Immunologic.
- immunology : Orthomyxoviridae, T-Lymphocytes, Cytotoxic.
- Animals, Complement Pathway, Alternative, Female, Hypersensitivity, Delayed, Mice, Mice, Inbred Strains.
Abstract
Gamma-inulin (g-IN) is a polymorph identified as the active component of inulin preparations that specifically activates the alternative pathway of complement (APC). The APC is central to many leucocyte functions, including B cell activation. We show here that g-IN, when formulated as a pure, endotoxin-free, fine suspension insoluble at 37 degrees C and given at 50-100 micrograms per mouse, is a potent adjuvant for both humoral and cell-mediated responses to a variety of antigens. g-IN increased secondary IgG responses five- to 28-fold (P less than 0.001), using as antigen phosphorylcholine coupled to keyhole limpet haemocyanin; subclasses IgG 2a, 2b, and 3 were boosted several hundred-fold, IgG 1 10-fold. IgM and IgA were increased four- to six-fold. Delayed hypersensitivity, by footpad swelling after secondary challenge with sheep red blood cells (SRBC), was increased more than two-fold (P less than 0.001) if g-IN was included with the primary SRBC, equivalent to increasing primary doses 10-fold. g-IN was equally active if given 5 days before the primary SRBC. Thus it is an immune stimulant rather than a depot or vehicle for antigen. Mice primed subcutaneously with 30-300 HA units of H2N2 influenza virus (strain A/JAP) and challenged intranasally with a lethal dose of H1N1 virus (strain A/WSN) all died, but if g-IN was given with the primary antigen 50% of the mice survived (P less than 0.001), a deduced but not proven boost to cytotoxic T cell-mediated immunity. Unpublished work has shown that g-IN has no adverse effects at adjuvant-active doses.(ABSTRACT TRUNCATED AT 250 WORDS)
DOI: 10.1038/icb.1988.45
PubMed: 3265692
Affiliations:
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Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adjuvants, Immunologic</term>
<term>Animals</term>
<term>Complement Pathway, Alternative</term>
<term>Female</term>
<term>Hemocyanins (immunology)</term>
<term>Hypersensitivity, Delayed</term>
<term>Immunoglobulins (biosynthesis)</term>
<term>Inulin (pharmacology)</term>
<term>Mice</term>
<term>Mice, Inbred Strains</term>
<term>Orthomyxoviridae (immunology)</term>
<term>T-Lymphocytes, Cytotoxic (immunology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adjuvants immunologiques</term>
<term>Animaux</term>
<term>Femelle</term>
<term>Hypersensibilité retardée</term>
<term>Immunoglobulines (biosynthèse)</term>
<term>Inuline (pharmacologie)</term>
<term>Lignées consanguines de souris</term>
<term>Lymphocytes T cytotoxiques (immunologie)</term>
<term>Orthomyxoviridae (immunologie)</term>
<term>Souris</term>
<term>Voie alterne d'activation du complément</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Immunoglobulins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Hemocyanins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Inulin</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Adjuvants, Immunologic</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Immunoglobulines</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lymphocytes T cytotoxiques</term>
<term>Orthomyxoviridae</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Orthomyxoviridae</term>
<term>T-Lymphocytes, Cytotoxic</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Inuline</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Complement Pathway, Alternative</term>
<term>Female</term>
<term>Hypersensitivity, Delayed</term>
<term>Mice</term>
<term>Mice, Inbred Strains</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Adjuvants immunologiques</term>
<term>Animaux</term>
<term>Femelle</term>
<term>Hypersensibilité retardée</term>
<term>Lignées consanguines de souris</term>
<term>Souris</term>
<term>Voie alterne d'activation du complément</term>
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<front><div type="abstract" xml:lang="en">Gamma-inulin (g-IN) is a polymorph identified as the active component of inulin preparations that specifically activates the alternative pathway of complement (APC). The APC is central to many leucocyte functions, including B cell activation. We show here that g-IN, when formulated as a pure, endotoxin-free, fine suspension insoluble at 37 degrees C and given at 50-100 micrograms per mouse, is a potent adjuvant for both humoral and cell-mediated responses to a variety of antigens. g-IN increased secondary IgG responses five- to 28-fold (P less than 0.001), using as antigen phosphorylcholine coupled to keyhole limpet haemocyanin; subclasses IgG 2a, 2b, and 3 were boosted several hundred-fold, IgG 1 10-fold. IgM and IgA were increased four- to six-fold. Delayed hypersensitivity, by footpad swelling after secondary challenge with sheep red blood cells (SRBC), was increased more than two-fold (P less than 0.001) if g-IN was included with the primary SRBC, equivalent to increasing primary doses 10-fold. g-IN was equally active if given 5 days before the primary SRBC. Thus it is an immune stimulant rather than a depot or vehicle for antigen. Mice primed subcutaneously with 30-300 HA units of H2N2 influenza virus (strain A/JAP) and challenged intranasally with a lethal dose of H1N1 virus (strain A/WSN) all died, but if g-IN was given with the primary antigen 50% of the mice survived (P less than 0.001), a deduced but not proven boost to cytotoxic T cell-mediated immunity. Unpublished work has shown that g-IN has no adverse effects at adjuvant-active doses.(ABSTRACT TRUNCATED AT 250 WORDS)</div>
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<name sortKey="Steele, E J" sort="Steele, E J" uniqKey="Steele E" first="E J" last="Steele">E J Steele</name>
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