Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1996-11-22
pubmed:abstractText
IL-4 is the critical regulatory cytokine that preferentially promotes a Th2 type of immune response. In certain models of organ-specific autoimmune diseases in which Th1 cells are implicated in the disease process, treatment with IL-4 has been shown to confer protection by deviating the immune response toward a Th2 type. In this study, we addressed the role of IL-4 in experimental autoimmune uveoretinitis, a prototypic Th1-dependent disease induced in susceptible animals following immunization with soluble retinal Ag. Interestingly, treatment of Lewis rats with IL-4 exacerbated experimental autoimmune uveoretinitis, and simultaneous treatment with neutralizing anti-IL-4 Abs attenuated this increase in the severity of the disease. Ex vivo analysis of cytokines produced in response to the immunizing Ag showed an enhancement in the levels of IFN-gamma, TNF-alpha, and nitric oxide following IL-4 treatment. In vitro, IL-4 augmented the production of IFN-gamma by Con A-stimulated splenocytes in a dose-dependent manner. At low concentrations of IL-4, IFN-gamma production was enhanced, while at higher concentrations this production was inhibited. The specificity of the induction of IFN-gamma by IL-4 was confirmed by neutralizing the activity of IL-4 with anti-IL-4. Taken together, the results herein reported demonstrate that IL-4 can induce the production of IFN-gamma and of inflammatory cytokines under certain conditions, and indicate that IL-4 can exert a dose-dependent differential effect on the induction of immune responses and on autoimmunity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adjuvants, Immunologic, http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies, http://linkedlifedata.com/resource/pubmed/chemical/Autoantigens, http://linkedlifedata.com/resource/pubmed/chemical/Eye Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II, http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Isotypes, http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4, http://linkedlifedata.com/resource/pubmed/chemical/Mercuric Chloride, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide, http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
157
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2209-15
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8757348-Adjuvants, Immunologic, pubmed-meshheading:8757348-Animals, pubmed-meshheading:8757348-Autoantibodies, pubmed-meshheading:8757348-Autoantigens, pubmed-meshheading:8757348-Dose-Response Relationship, Drug, pubmed-meshheading:8757348-Eye Proteins, pubmed-meshheading:8757348-Female, pubmed-meshheading:8757348-Histocompatibility Antigens Class II, pubmed-meshheading:8757348-Immunoglobulin Isotypes, pubmed-meshheading:8757348-Interferon-gamma, pubmed-meshheading:8757348-Interleukin-4, pubmed-meshheading:8757348-Male, pubmed-meshheading:8757348-Mercuric Chloride, pubmed-meshheading:8757348-Nitric Oxide, pubmed-meshheading:8757348-Rats, pubmed-meshheading:8757348-Rats, Inbred BN, pubmed-meshheading:8757348-Rats, Inbred Lew, pubmed-meshheading:8757348-Recombinant Proteins, pubmed-meshheading:8757348-Retina, pubmed-meshheading:8757348-Retinitis, pubmed-meshheading:8757348-Tumor Necrosis Factor-alpha, pubmed-meshheading:8757348-Uveitis
pubmed:year
1996
pubmed:articleTitle
Recombinant IL-4 aggravates experimental autoimmune uveoretinitis in rats.
pubmed:affiliation
INSERM Unit 430, Broussais Hospital, Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't