Why does late-onset asthma seem to encourage higher risk of heart disease and stroke? The researchers theorize that the nuanced differences between early and late-onset seem to be at play here. In addition to the heightened difficulty of controlling late-onset asthma with standard medications that typically resolve early-onset flare ups, late-onset asthma may be specifically linked to air pollution and often involves a more rapid decline of lung function. A 2012 study published in the European Journal of Heart Failure links airflow obstruction and compromised lung function with a higher risk of incident heart failure. Limitations of the study include the fact that most of the subjects were Caucasian, and details on air pollution exposure and stressful life events, which can raise heart disease risk, were not accessible.
The role of adaptive immune responses mediated by antigen specific Th17 has been investigated more recently. Antigen specific Th17 cells were also shown to recognize conserved protein antigens among different K. pneumoniae strains and provide broad-spectrum serotype-independent protection.  Antigen specific CD4 T cells also limit nasopharyngeal colonization of S. pneumoniae in mouse models.  Furthermore, immunization with pneumococcal whole cell antigen and several derivatives provided IL-17-mediated, but not antibody dependent, protection against S. pneumoniae challenge.   In fungal infection, it has been shown an IL-17 producing clone with a TCR specific for calnexin from Blastomyces dermatitidis confers protection with evolutionary related fungal species including Histoplasma spp.