Summary and conclusions
Understanding the basis of widespread heterogeneity in the
manifestations of CRS is advanced by findings that the three main
endotypes, T1, T2 and T3, orchestrate the expression of three distinct
large sets of genes. It is clear that T2 inflammation can be found
around the world and in both CRSwNP and CRSsNP phenotypes. Although the
prevalence of T2 endotype in Asia was very low decades ago, it is
increasing with industrialization. Another emerging view is that
endotype, rather than the phenotype, can drive clinical features, such
as the presence of comorbid asthma (T2sNP and T2wNP) and pus (T3sNP and
T3wNP). Drugs blocking T2 inflammation can shrink nasal polyps in
western countries; as trials are initiated in T2sNP patients, we expect
that this very large group of patients will be found to benefit from
blockade of type 2 inflammation. Studies of the microbiome may discover
that the higher prevalence of T3 forms of CRS in China reflect distinct
microbiological exposures. The development and use of improved methods
of endotyping disease in the clinic will likely usher in expansion of
the use of biological therapies targeting T2 and introduction of
treatments targeting other endotypes.