TY - JOUR
T1 - Pathophysiologic mechanisms of chronic rhinosinusitis and their roles in emerging disease endotypes
AU - Cao, Ping Ping
AU - Wang, Zhi Chao
AU - Schleimer, Robert P.
AU - Liu, Zheng
N1 - Funding Information:
Funding Sources: This work was supported by the National Natural Science Foundation of China (grant 81400449 to P.-P.C. and grants 81630024 , 81570899 , and 81325006 to Z.L.), the Natural Science Foundation of Hubei Province (grant 2017CFA016 to Z.L.), and the “Ten Thousand Plan” of the National High Level Talents Special Support Plan (to Z.L.). R.P.S was supported in part by grants R37HL068546, AI137174, and U19AI106683 (Chronic Rhinosinusitis Integrative Studies Program [CRISP]) from the National Institutes of Health and The Ernest S. Bazley Charitable Foundation.
Publisher Copyright:
© 2018 Elsevier Ltd
PY - 2019/1
Y1 - 2019/1
N2 - Objective: Chronic rhinosinusitis (CRS) is a heterogeneous disorder with distinct pathophysiologic mechanisms. Based on transcription factor expression and cytokine production patterns in different innate lymphoid cell (ILC) types, in parallel with those of adaptive CD4+ T-helper (TH) cells and CD8+ cytotoxic T (Tc) cells, new perspectives on endotypes of patients are emerging for the immune response deviation into type 1 (orchestrated by ILC1s and Tc1, and TH1 cells), type 2 (characterized by ILC2s and Tc2 and TH2 cells), and type 3 (mediated by ILC3s and Tc17 and TH17 cells). In addition, cluster analysis has been applied to endotyping of CRS in recent years, which has provided additional novel insights into CRS pathogenesis. This review assessed pathologic mechanisms of CRS based on type 1, 2, and 3 immune responses and how they inform us to begin to understand CRS endotypes. This review also assessed recent cluster analysis studies of CRS endotypes. The impact of endotype on therapeutic management of CRS also is summarized. Data Sources: Review of published literature. Study Selections: Relevant literature concerning CRS endotypes and possible underlying mechanisms was obtained from a PubMed search and summarized. Results and Conclusion: CRS with and without nasal polyps are composed of distinct endotypes with distinct deviated immune responses, pathogenic mechanisms, and different responses to medical and surgical treatment. An endotype of CRS with prominent type 2 immune responses is the best-studied endotype and generally can benefit from treatment with steroids and specific type 2 disrupting biologics.
AB - Objective: Chronic rhinosinusitis (CRS) is a heterogeneous disorder with distinct pathophysiologic mechanisms. Based on transcription factor expression and cytokine production patterns in different innate lymphoid cell (ILC) types, in parallel with those of adaptive CD4+ T-helper (TH) cells and CD8+ cytotoxic T (Tc) cells, new perspectives on endotypes of patients are emerging for the immune response deviation into type 1 (orchestrated by ILC1s and Tc1, and TH1 cells), type 2 (characterized by ILC2s and Tc2 and TH2 cells), and type 3 (mediated by ILC3s and Tc17 and TH17 cells). In addition, cluster analysis has been applied to endotyping of CRS in recent years, which has provided additional novel insights into CRS pathogenesis. This review assessed pathologic mechanisms of CRS based on type 1, 2, and 3 immune responses and how they inform us to begin to understand CRS endotypes. This review also assessed recent cluster analysis studies of CRS endotypes. The impact of endotype on therapeutic management of CRS also is summarized. Data Sources: Review of published literature. Study Selections: Relevant literature concerning CRS endotypes and possible underlying mechanisms was obtained from a PubMed search and summarized. Results and Conclusion: CRS with and without nasal polyps are composed of distinct endotypes with distinct deviated immune responses, pathogenic mechanisms, and different responses to medical and surgical treatment. An endotype of CRS with prominent type 2 immune responses is the best-studied endotype and generally can benefit from treatment with steroids and specific type 2 disrupting biologics.
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U2 - 10.1016/j.anai.2018.10.014
DO - 10.1016/j.anai.2018.10.014
M3 - Review article
C2 - 30326322
AN - SCOPUS:85056662166
VL - 122
SP - 33
EP - 40
JO - Annals of Allergy, Asthma and Immunology
JF - Annals of Allergy, Asthma and Immunology
SN - 1081-1206
IS - 1
ER -