No abstract available.
Animals ; Interleukin-4* ; Mice*

No abstract available.
Interleukin-4* ; Interleukins* ; Receptors, Interleukin-4* ; Rheumatic Diseases*

No abstract available.
Child* ; Humans ; Hypersensitivity ; Interleukin-4*

Asthma is a chronic allergic inflammatory disease of lung. The initiation and progression of asthma is dependent on the cytokines interleukin (IL) -4 and IL-13 acting through related receptor complexes. Disease pathogenesis is effected by intracellular signaling pathways that couple primarily to specific motifs within the intracellular domain of the IL-4 receptor alpha chain (IL-4R alpha), a subunit that is common to the IL-4 and IL-13 receptor complexes. Neutralizing anti-cytokine strategies have proven to be highly successful on dissecting relevant effector pathways in experimental allergic disease, and are now entering clinical trials in human allergic disorders. Although there have been only a few clinical studies on the effects of cytokine modulators in asthma, this line of research and development appears promising.
Asthma* ; Cytokines ; Humans ; Interleukin-13 ; Interleukin-4 ; Interleukins ; Lung ; Receptors, Interleukin-13 ; Receptors, Interleukin-4

Dexamethasone is a widely used anti-inflammatory agent for a broad spectrum of diseases. The effectiveness of this agent is thought to be due to the capacity to modulate cytokine production in inflammatory cells. We examined the effects of dexamethasone on expressions of interferon gamma (IFN-gamma) and interleukin 4 (IL-4) by human peripheral blood mononuclear cells (PBMCs) in response to interleukin 12 (IL-12). Dexamethasone (10-5 M) inhibited IFN-gamma secretion, through direct suppression of IFN-gamma, IL-12 receptor (IL-12R) -beta1, and -beta2 expressions. Conversely dexamethasone increased IL-4 secretion as well as IL-4 expressions by PBMCs in response to IL-12. In addition, dexamethasone increased expression of suppressor of cytokine signalling (SOCS)-1, which inhibits JAK-STAT pathway of IL-12R signalling. The result of our study suggested that dexamethasone directly inhibited IFN-gamma expression, through suppression of IL-12 signalling and indirectly increases IL-4 expression, through suppression of IFN-gamma expression.
Dexamethasone* ; Humans ; Interferons ; Interleukin-12* ; Interleukin-4* ; Receptors, Interleukin-12

BACKGROUND: The human keratinocyte can synthesize interleukin 6 (IL-6) under certain conditions, and the IL-6 synthesis is inhibited by interleukin 4 (IL-4) in the human monocyte. OBJECTIVE: To find out what kind of stimulating agents can induce the IL-6 production and whether IL-4 affects the production of IL-6 in the human cultured keratinocytes. METHODS: We stimulated the keratinocytes with either lipopolysaccharide (LPS), fetal bovine serum (FBS), human recombinant interferon-gamma(IFN-gamma) to induce the IL-6 production, and treated the keratinocytes, which stimulated either with 10% FBS or human recombinant IFN-gamma, with human recombinant IL-4. RESULTS: The LPS stimulation resulted in no increase of IL-6 levels in the keratinocyte supernatants. When the keratinocytes were stimulated either with 1%, 5%, 10% FBS with or without 5 microgram/ml LPS, significantly increased amounts of IL-6 were detected. The level of IL-6 in the keratinocytes treated with the human recombinant IFN-gamma increased, too. The human recombinant IL-4 downregulates the secretion of IL-6 by the keratinocytes which were activated either with 10% FBS or human recombinant IFN-gamma. CONCLUSION: We have shown that it is possible to induce the IL-6 synthesis by stimulating the keratinocytes and that human recombinant IL-4 profoundly inhibits the synthesis of IL-6. So we suggest that there may be a cytokine network which regulates the primary immune response in the skin.
Humans* ; Interleukin-4* ; Interleukin-6* ; Interleukins* ; Keratinocytes* ; Monocytes ; Skin

T helper-type 2 cytokines, such as IL-4 and IL-13, may play a central role in allergic diseases. The protein known as signal transducers and activators of transcription 6 (STAT6) is a key transcription factor involved in both IL-4- and -13-mediated biological responses. Two polymorphisms of the STAT 6 gene (exon 1 and G2964A variant) have been found. We investigated whether these STAT6 gene polymorphisms were associated with allergic rhinitis. Blood samples for genetic analysis were obtained from 285 individuals with allergic rhinitis and from 271 healthy subjects without atopic disease. The G2964A variant of the STAT6 gene was genotyped using PCR-RFLP analysis. The GT repeat polymorphism in exon 1 of the STAT6 gene was genotyped by fragment analysis. There was no association between the 2964A variant and GT repeat polymorphism in exon 1 of the STAT6 and allergic rhinitis in a Korean population (both p > 0.05). Our results suggest that a combination of STAT6 gene polymorphisms is not a useful marker for predicting allergic rhinitis.
Cytokines ; Exons ; Interleukin-13 ; Interleukin-4 ; Rhinitis* ; Transcription Factors ; Transducers

To investigate the imbalance of the cytokine production profile of T cells from atopic asthmatics, we measured concentrations of IL-4, IL-5 and IFN-y by ELISA method in the culture supernatants of peripheral blood mononuclear cells(PBMCs) and Derrnato-phagoides pteronyssinus(Der p) J-stimulated PBMCs from Der p-sensitized atopic asthmatics, Der p-sensitized healthy atopits, non-atopic asthmatics and healthy non-atopics. The suppressive effect of IFN-y on cytokine production of Der p J-stimulated PBMCs was also examined. The PBMCs from atopics showed higher IL-4 and IL-5 production in response to PHA +TPA and higher IFN-gamma production in response to Der p Jq compared with non-atopits. The Der p J-stimulated PBMCs from atopics showed a tendency of increased IL-5 production in response to Der p J and higher IL-4 and IL-5 production in response to PHA+TPA compared with non-atopics. IL-5 production of Der p J-stimulated PBMCs from atopics was suppressed by IFN It is suggested that an imbalance in IL-4, IL-5 and IFN-y production is a feature of the atopic state. The TH2 characteristics of allergen-stimulated PBMCs could be regulated by IFN-y.
Enzyme-Linked Immunosorbent Assay ; Interleukin-4 ; Interleukin-5 ; T-Lymphocytes

Objectives: Cytokines are critical regulatory molecules that circulate in blood at measurable levels. However, the epidemiology of serum cytokine levels in healthy populations is still limited, particularly for Japanese populations. The objective of this study was to examine the relation between serum cytokine levels and common laboratory tests in a healthy Japanese population. Methods: We studied serum levels of six cytokines (interleukin-4 (IL-4), IL-5, IL-6, IL-10, interferon-γ (IFN-γ), granulocyte-macrophage colony-stimulating factor (GM-CSF)) in a healthy Japanese population using a sensitive chemiluminescence ELISA (CL-ELISA). We examined the relations between serum cytokine levels and common laboratory tests using multiple regression analysis. We were particularly interested in potential relations between serum cytokine levels and C-reactive protein (CRP) in light of its relation to the risk of cardiovascular events. We also investigated the relation between cytokine levels, alcohol consumption and smoking. Results: After adjusting for the influence of other cytokines and laboratory tests, the serum level of IL-4 was associated with IL-5 and GM-CSF. In addition to IL-4, IL-5 was also associated with IL-10 and IFN-γ. IL-6 was associated with IL-10 and IFN-γ, and IL-10 and IFN-γ were associated with GM-CSF. CRP was significantly negatively associated with serum IL-4 level. IL-6 was weakly correlated with alcohol consumption level in this population. IL-5 among smokers tended to be lower than that among nonsmokers. Conclusions: Close relations among serum cytokine levels were observed in a healthy population. It is interesting that the level of IL-4, an anti-inflammatory cytokine, was inversely related to CRP level, suggested to be a marker of inflammation.
Serum ; Cytokines ; Interleukin-4 ; Japanese language ; Interleukin-10

BACKGROUND: A small subgroup of atopic dermatitis (AD) patients show low total and allergen-specific immunoglobulin (IgE) levels. This subgroup has been termed 'intrinsic' AD (IAD) as compared to its counterpart 'extrinsic' AD (EAD). However, the difference of cytokine expression between IAD and EAD has not been fully understood. OBJECTIVE: To compare the expression of various inflammatory cytokines in the peripheral blood mononuclear cells (PBMCs) and lesional skin of patients with IAD and EAD, which are known to be associated with AD pathophysiology. METHODS: We assessed the protein levels of cytokines in the PBMCs and lesional skin. We evaluated the levels of IL-3, IL-4, IL-5, IL-6, IL-10, IL-13, FcepsilonRI and FcepsilonRII from the PBMCs and lesional skin of patients with IAD and EAD. RESULTS: The patients with EAD had elevated levels of the IL-3 expression in their PBMCs and elevated levels of FcepsilonRI in their lesional skin compared to that of the patients with IAD. The expression of other cytokines did not differ in the PBMCs and lesional skin from the two subgroups. CONCLUSION: This study suggests that IL-3 could be associated with the pathophysiology of EAD as compared to that of IAD, along with FcepsilonRI which was previously shown to be highly expressed in EAD patients.
Cytokines ; Dermatitis, Atopic ; Humans ; Immunoglobulins ; Interleukin-10 ; Interleukin-13 ; Interleukin-3 ; Interleukin-4 ; Interleukin-5 ; Interleukin-6 ; Skin