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Neutralization of interleukin-17 suppresses allergic rhinitis symptoms by downregulating Th2 and Th17 responses and upregulating the Treg response.
Oncotarget. 2017 Apr 04; 8(14):22361-22369.O

Abstract

Allergic rhinitis (AR) has long been considered to predominantly involve the actions of Th2 cells, with relatively small contributions from Th1 cells. In recent years, the discovery of Th17 and regulatory T (Treg) cells has rendered the Th1/Th2 balance paradigm more complex and expanded our understanding of the pathogenesis of AR. IL-17, a key cytokine produced by Th17 cells, is known to induce allergen-specific Th2 cell activation, eosinophil and neutrophil accumulation, and serum IgE production in asthma; all of these features may play important roles in AR. To the best of our knowledge, only a few studies have assessed the feasibility of using IL-17 antagonists to treat AR. Thus, the principal objectives of the present study were, first, to determine the status of Th17 and Treg cells in the nasal mucosa of a mouse model of AR, and, second, to investigate the effects of IL-17 on such cells and the therapeutic efficacy of anti-IL-17 antibodies (Abs) in the context of AR. Anti-IL-17 Abs were given intranasally during the re-challenge of BALB/c mice with ovalbumin (OVA)-induced AR. We measured the numbers of nasal rubbing motions and sneezes, eosinophil and neutrophil levels, Th1, Th2, Th17, and Treg parameters in the nasal mucosa. Anti-IL-17 Abs markedly reduced the number of nasal rubbing motions and sneezes, decreased eosinophil and neutrophil infiltration, reduced Th2 and Th17 responses, and increased the Treg response. Anti-IL-17 Ab treatment protects against AR. These results will improve our understanding of AR pathogenesis and may lead to the development of novel therapeutic approaches for management of the condition.

Authors+Show Affiliations

Department of Otorhinolaryngology, China Medical University Affiliated Shengjing Hospital, Shenyang, Liaoning, China.Department of Medical Insurance, China Medical University Affiliated Shengjing Hospital, Shenyang, Liaoning, China.Department of Otorhinolaryngology, China Medical University Affiliated Shengjing Hospital, Shenyang, Liaoning, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28423590

Citation

Gu, Zhao Wei, et al. "Neutralization of Interleukin-17 Suppresses Allergic Rhinitis Symptoms By Downregulating Th2 and Th17 Responses and Upregulating the Treg Response." Oncotarget, vol. 8, no. 14, 2017, pp. 22361-22369.
Gu ZW, Wang YX, Cao ZW. Neutralization of interleukin-17 suppresses allergic rhinitis symptoms by downregulating Th2 and Th17 responses and upregulating the Treg response. Oncotarget. 2017;8(14):22361-22369.
Gu, Z. W., Wang, Y. X., & Cao, Z. W. (2017). Neutralization of interleukin-17 suppresses allergic rhinitis symptoms by downregulating Th2 and Th17 responses and upregulating the Treg response. Oncotarget, 8(14), 22361-22369. https://doi.org/10.18632/oncotarget.15652
Gu ZW, Wang YX, Cao ZW. Neutralization of Interleukin-17 Suppresses Allergic Rhinitis Symptoms By Downregulating Th2 and Th17 Responses and Upregulating the Treg Response. Oncotarget. 2017 Apr 4;8(14):22361-22369. PubMed PMID: 28423590.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neutralization of interleukin-17 suppresses allergic rhinitis symptoms by downregulating Th2 and Th17 responses and upregulating the Treg response. AU - Gu,Zhao Wei, AU - Wang,Yun Xiu, AU - Cao,Zhi Wei, PY - 2016/03/02/received PY - 2017/02/15/accepted PY - 2017/4/21/entrez PY - 2017/4/21/pubmed PY - 2017/9/16/medline KW - Immune response KW - Immunity KW - Immunology and Microbiology Section KW - Th17 KW - Th2 KW - allergic rhinitis KW - interleukin-17 KW - neutralization SP - 22361 EP - 22369 JF - Oncotarget JO - Oncotarget VL - 8 IS - 14 N2 - Allergic rhinitis (AR) has long been considered to predominantly involve the actions of Th2 cells, with relatively small contributions from Th1 cells. In recent years, the discovery of Th17 and regulatory T (Treg) cells has rendered the Th1/Th2 balance paradigm more complex and expanded our understanding of the pathogenesis of AR. IL-17, a key cytokine produced by Th17 cells, is known to induce allergen-specific Th2 cell activation, eosinophil and neutrophil accumulation, and serum IgE production in asthma; all of these features may play important roles in AR. To the best of our knowledge, only a few studies have assessed the feasibility of using IL-17 antagonists to treat AR. Thus, the principal objectives of the present study were, first, to determine the status of Th17 and Treg cells in the nasal mucosa of a mouse model of AR, and, second, to investigate the effects of IL-17 on such cells and the therapeutic efficacy of anti-IL-17 antibodies (Abs) in the context of AR. Anti-IL-17 Abs were given intranasally during the re-challenge of BALB/c mice with ovalbumin (OVA)-induced AR. We measured the numbers of nasal rubbing motions and sneezes, eosinophil and neutrophil levels, Th1, Th2, Th17, and Treg parameters in the nasal mucosa. Anti-IL-17 Abs markedly reduced the number of nasal rubbing motions and sneezes, decreased eosinophil and neutrophil infiltration, reduced Th2 and Th17 responses, and increased the Treg response. Anti-IL-17 Ab treatment protects against AR. These results will improve our understanding of AR pathogenesis and may lead to the development of novel therapeutic approaches for management of the condition. SN - 1949-2553 UR - https://www.unboundmedicine.com/medline/citation/28423590/Neutralization_of_interleukin_17_suppresses_allergic_rhinitis_symptoms_by_downregulating_Th2_and_Th17_responses_and_upregulating_the_Treg_response_ L2 - http://www.impactjournals.com/oncotarget/misc/linkedout.php?pii=15652 DB - PRIME DP - Unbound Medicine ER -