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Dr. Domenico Fiore: studi e ricerche sulla pertosse Dr. Domenico FIORE
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An Ipothesis of its Aetiopathogenesis. A need for verification

(Published by "EOS" Journal of Immunology and Immunopharmacology. Vol. XXIII - 2003 - n. 3-4 - 81-94)

Studing the neurophaties from Bordetella Pertussis (experimental allergic encephalitis, multiple sclerosis, amyotrophic lateral sclerosis; correlated neuropathies) it came out that in all the animals (human being included) the factor that conditions the emergence of any clinical form (neurophaties with patches; neurophaties without patches) is represented by the fenotype of astrocytes that can be producers, or non-producers of II class antigens-HLA.

Ri-examining all the anatomopathological and immunological aspects of the most common “autoimmune diseases” I had the impression that the fenotype “tissue-specific Antigen Presenting Cells (APCs) producers or non-producers of II class Ags-HLA” is not restricted only at the Central Nervous System (CNS). If in every organs the local APCs (tissue specific) can be producers, or non-producers of II class Ags-HLA, conditioning the possibility that in that organ the precipitation of casual circulating immune complexes occurs or not, it would follow that in subjects with mucus ciliary barrier defect (condicio sine qua non) the infection caused by an infectious agent provided with a strong aspecific polyclonal activator capacity of B-lymphocytes and a mitogen capacity on T-lymphocytes, would induce, in circulating blood, activation and mitogenesis to arrive at T-lymphocytes autocytotoxicity and at B-lymphocytes specific and aspecific polyclonal activation with production also of autoantibodies (autoimmunity). We could have:

A) In those subjects in whom the tissular APCs of a certain organ are II class Ags-HLA producers: the CIC “will irritate” the small blood vessel walls; the microvasal endothelium will expose the adhesion molecules; the local APCs will expose the exogenous antigen (the bacteriotoxins) in the II class antigens-HLA context. This way we will arrive at a “stable adhesion”; after that the precipitation of the CIC and the direct contact of T-cells (become autocytotoxic) with the specific cells of that organ, will follow. There will be: - CIC depositions; Cytokines production; lymphomonocytic infiltrations; - “direct contact” of activated lymphocytes with the membrane antigens of cells normally not exposed. We will have autocytotoxicity and autoantibodies turned against that organ: 'Organ-Specific Autoimmune Diseases' (Nervous Central System in the SM; Thyroid in Basedow Disease; Thimus in Myasthenia Gravis; Stomach; Pancreas; Parathyroid; Adrenal Gland).

B) In those subjects in whom, in several organs, the tissular APCs are producers of II class Ags-HLA and there are the propitious anatomic conditions to a frequent slowing down of the hematic flow (see: endocrine glands anatomy) the phenomenons described above in A) will favour the CIC precipitation and the direct contact of T-cells (become autocytotoxic) with the glandular epithelium. In this case we could have “Polyendocrine Syndromes”.

C) In those subjects in whom the tissular (fixed) APCs are not II class Ags-HLA producers: we will not have the circulating immune complexes precipitation; there will not be direct contact between the activated immunocompetent cells and the antigens of cells usually not exposed. We will have the “Non Organ-specific Autoimmune Diseases” (LES; Monoclonal Gammapathies).

D) In those subjects in whom the APCs of some districts, expose the II class Antigens-HLA only as a response to a very severe irritant stimulus (see the text: responder and non responder; genetic and factors that can influence the immune response entity), we will have “Autoimmune Mixed Diseases (Intermediate forms)” in which, together with the typical symptoms of non organ-specific forms (CIC; autoantibodies), there will be the autoimmune damage of a non specific tissue of an organ (Connectivitis; Scleroderma).

To check what I have explained above, I have studied nine patients whose clinical diagnosis were: LES (3 cases); Scleroderma (2 cases); Monoclonal Gammapathy (2 cases); MGUS, gammapathy of uncertain significance (2 cases). In all those cases, the anti Bordetella antibodies reserch, practiced with the Pesaro method (see text), has resulted clamourously positive.

Considering the individual and social benefits that in these diseases would follow from the availability of a precocious etiologic diagnosis (easy with an adeguate method) and from the availability of an effectual specific therapy, it is strongly required an objective verification by all doctors.

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Last update: June 2004