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Human papillomaviruses (HPV) include a large family of viruses that are considered to be part of the normal flora of the human epithelium. However, the activation of these pathogenic agents leads to the formation of warts of the skin or papillomas of the mucous membranes. However, in most immunocompetent people, the virus remains latent. Patients with papillomatosis of the larynx (LP) and respiratory tract often have multiple relapses of the disease, which indicates the inability of their immune systems to inhibit the multiplication of the virus and is likely to be the result of complex and local immunosuppression. Indeed, a large list of works in which immune cells are studied at the sites of lesion describes defects in Langerhans cells (LC), an increase in the number of regulatory T-lymphocytes (Treg), the predominance of differentiation of T-helper cells into the Th2 type, and natural killer cell dysfunction (NK) and B-lymphocytes. But to date, there is no complete overview of the mechanism of immunosuppression in papillomas caused by HPV 6 and 11.

Systemic and local changes in the immunological status of patients with laryngeal papillomatosis