The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Proinflammatory cytokines (IL-17, IL-6, IL-18 and IL-12) and Th cytokines (IFN-γ, IL-4, IL-10 and IL-13) in patients with allergic asthma
Open accessAbstract
Summary: Allergen-reactive T helper type-2 (Th2) cells and proinflammatory cytokines have been suggested to play an important role in the induction and maintenance of the inflammatory cascade in allergic asthma. We compared the plasma concentrations of novel proinflammatory cytokines IL-17 and IL-18, other proinflammatory cytokines IL-6 and IL-12, Th2 cytokines IL-10 and IL-13, and intracellular interferon-γ (IFN-γ) and IL-4 in Th cells of 41 allergic asthmatics and 30 sex- and age-matched health control subjects. Plasma cytokines were measured by enzyme-linked immunosorbent assay. Intracellular cytokines were quantified by flow cytometry. Plasma IL-18, IL-12, IL-10, IL-13 concentrations were significantly higher in allergic asthmatic patients than normal control subjects (IL-18: median 228·35 versus 138·72 pg/ml, P < 0·001; IL-12: 0·00 versus 0·00 pg/ml, P = 0·001; IL-10: 2·51 versus 0·05 pg/ml, P < 0·034; IL-13: 119·38 versus 17·89 pg/ml, P < 0·001). Allergic asthmatic patients showed higher plasma IL-17 and IL-6 concentrations than normal controls (22·40 versus 11·86 pg/ml and 3·42 versus 0·61 pg/ml, respectively), although the differences were not statistically significant (P = 0·077 and 0·053, respectively). The percentage of IFN-γ-producing Th cells was significantly higher in normal control subjects than asthmatic patients (23·46 versus 5·72%, P < 0·001) but the percentage of IL-4 producing Th cells did not differ (0·72 versus 0·79%, P > 0·05). Consequently, the Th1/Th2 cell ratio was significantly higher in normal subjects than asthmatic patients (29·6 versus 8·38%, P < 0·001). We propose that allergic asthma is characterized by an elevation of both proinflammatory and Th2 cytokines. The significantly lower ratio of Th1/Th2 cells confirms a predominance of Th2 cells response in allergic asthma.
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Cited by
IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis
Komiyama, Y., Nakae, S., Matsuki, T., Nambu, A., Ishigame, H., Kakuta, S., Sudo, K., & Iwakura, Y. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.1.566 · Cited by 1,536
Type 2 immunity in tissue repair and fibrosis
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IL-6 signal transduction and its physiological roles: the signal orchestration model
Kamimura, D., Ishihara, K., & Hirano, T. (2003) · Reviews of Physiology, Biochemistry and Pharmacology · doi:10.1007/s10254-003-0012-2 · Cited by 673
Wong, C. K., Lit, L. C. W., Tam, L. S., Li, E. K. M., Wong, P. T. Y., & Lam, C. W. K. (2008) · Clinical Immunology · doi:10.1016/j.clim.2008.01.019 · Cited by 532
Self-citationThe roles of IL‐17A in inflammatory immune responses and host defense against pathogens
Iwakura, Y., Nakae, S., Saijo, S., & Ishigame, H. (2008) · Immunological Reviews · doi:10.1111/j.1600-065x.2008.00699.x · Cited by 513
Metadata
- Authors
- Wong, C. K., Ho, C. Y., Ko, F. W. S., Chan, C. H. S., Ho, A. S. S., Hui, D. S. C., & Lam, C. W. K.
- Venue
- Clinical and Experimental Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2001-08
- Volume
- 125
- Issue
- 2
- Pages
- 177-183
- ISSN
- 0009-9104 (ISSN-L)
- 1365-2249
- OpenAlex
- W2060769801
- Cited by
- 440
- References
- 36
- FWCI
- 6.82
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Proinflammatory cytokines (IL-17, IL-6, IL-18 and IL-12) and Th cytokines (IFN-γ, IL-4, IL-10 and IL-13) in patients with allergic asthma. https://app.cochat.ai/papers/10.1046/j.1365-2249.2001.01602.x
- The paper
- Wong, C. K., Ho, C. Y., Ko, F. W. S., Chan, C. H. S., Ho, A. S. S., Hui, D. S. C., & Lam, C. W. K. (2001). Proinflammatory cytokines (IL-17, IL-6, IL-18 and IL-12) and Th cytokines (IFN-γ, IL-4, IL-10 and IL-13) in patients with allergic asthma. Clinical and Experimental Immunology. https://doi.org/10.1046/j.1365-2249.2001.01602.x
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