Yohannes Negesse
Centre Hospitalier Universitaire de la Guadeloupe, France
Title: Hanseniasis as a model of non-idiopathic polygenic autoimmune and autoinflammatory diseases
Biography
Biography: Yohannes Negesse
Abstract
Applied to hanseniasis Antoine Béchamp stipulation “the microbe is nothing, the terrain is everything” may be considered as a link between the eras before and after A. Hansen. Regarding hanseniasis the widely accepted classification was formulated by Ridley and Jopling (1966). This classification divided this disease into two stable polar forms with instable borderline in between the two. This classification was based on bacteriological, immunological, histopathological and clinical features of the disease caused by M. leprae infection. O. Wagner (1969) forwarded the observations that in hanseniasis “many responses of the host are similar to those described as typical of the so-called collagen diseases”. J.L. Turk published (1976) his paper entitled “Leprosy as a model of subacute and chronic immunologic diseases”. The role of the adaptive and innate immunities in hanseniasis has been underlined by numerous publications since these initial papers. By deduction we see that hanseniasis comes within the scope of the immunological diseases classification proposed by D. McGonagle and M. McDermott (2006). The tuberculoid and lepromatous poles of Ridley-Jopling classification correspond respectively to the polygenic autoimmune and polygenic autoinflammatory poles of McGonagle-McDermott classification. Curiously, M. leprae has an exclusive ability to infect Schwann cells in peripheral nerves. Therefore the initial interaction between M. leprae and macrophages process is decisive for the outcome of the disease. This is to say that the initial bacillary load within the nerve is an essential factor determining the cycle and spectrum of hanseniasis.