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Air pollution may promote type 2 diabetes by increasing adipose inflammation and insulin resistance.

Arsenic may promote type 2 diabetes by increasing insulin resistance (inability to utilize insulin at the cellular level) and impairing insulin production.

Thus, chitin-elicited activation of ILC2s may promote type 2 immune response and airway eosinophilia while it may suppress γδT cell-mediated neutrophilic airway inflammation.

Also, insulin resistance is affected by oxidative stress and, when combined with up regulated NF-κB activity, may promote type 2 diabetes.

Even though the role of prolactin in psoriasis is not completely clear [ 17, 18], recent studies suggest that it may enhance IFN-gamma-induced CXCL9, CXCL10, and CXCL11 production in keratinocytes via activation of STAT1, NF-kappaB, and IRF-1 through the JAK2 and MEK/ERK pathways and thus may promote type 1 T-cell infiltration into psoriatic lesions [ 19].

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Findings from a study conducted by Brook et al. (2008) have suggested that several of the biological pathways that have been linked to air pollution and cardiovascular disease (including systemic oxidative stress and low-grade inflammation) may also promote type 2 diabetes.

However, solitary foraging seems to characterize almost all nocturnal primates irrespective of their diet, suggesting that factors other than feeding competition may promote this type of social organization [Schülke, 2003].

There is some evidence that infections may promote certain types of cancers (Kuper et al, 2000).

In Brca1-deficient cells, Moynahan et al [ 12] believe that nonhomologous processes may promote aberrant types of repair.

If cross-immunity exists between HPV types, a vaccine that reduces the prevalence of 1 type may promote the prevalence of other types through a process of competitive release.

Some research has shown that the blood is more prone to clotting in the morning, which may promote the second type of stroke and inhibit the first.

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