Pertussis toxin other lung cells produce a variety of chemokines. PT has been found to inhibit the early transcription of keratinocyte-derived chemokine, macrophage inflammatory protein 2 and LPS-induced CXC chemokine. Eventually, PT causes lymphocytosis, one of the systemic manifestations of whooping cough. PT, a decisive virulence determinant of "B. pertussis", is able to cross the blood–brain barrier by increasing its permeability. As a result, PT can cause severe neurological complications; however, recently it has been found that the medicinal usage of "Pertussis" toxin can promote the development of regulatory T cells and prevent central nervous system autoimmune disease, such as multiple sclerosis.
Vogt–Koyanagi–Harada disease at the University of Tokyo, in 1911. It was the much later article, published in 1929, that definitively associated Koyanagi with the disease. Harada's 1926 paper is recognized for its comprehensive description of what is now known as Vogt–Koyanagi–Harada disease. Vogt–Koyanagi–Harada disease Vogt–Koyanagi–Harada disease (VKH), also known as Vogt–Koyanagi–Harada syndrome, uveomeningitis syndrome and uveomeningoencephalitic syndrome, is a multisystem disease of presumed autoimmune cause, that affects pigmented tissues, which have melanin. The most significant manifestation is bilateral, diffuse uveitis, which affects the eye. VKH may variably also involve the inner ear with effects on hearing, the skin, and the meninges of