Publication: Immunolocalization of cell-wall-deficient f orms of Mycobacterium tuberculosis com plex in sarcoidosis and in sinus histiocytosis of lymph nodes draining carcinoma
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Date
1996
Authors
Alavi, H.A. ; Moscovic, E.A.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
In sarcoidosis, pleomorphic chromogens
(PCs) occur as multivariate pigmented elements within
sinusoids of lymph nodes (sinusoidal phase) and as tiny
«round bodiesm detectable in granulomas (generalized
phase). The sinusoidal phase occurs in other conditions
as well and characteristically contains yeastlike bodies
also known as H-W bodies. To elucidate the antigenic
profile of al1 variant forms, 28 cases of sarcoidosis
(series A) and 14 cases of malignancy associated sinus
histiocytosis (series B) were studied immunohistochemically
with panels of various antibodies, including
antimycobacterial MAbs specific for M. tuberculosis
complex (TB68, TB71), for M. leprae (MMP-1-3C3) and
for cross-reactive mycobacterial antigens (F24-2-3 and
F116-5, the latter recognizing superoxide dismutase).
Results for series A indicate that: 1) PCs are cell-walldeficient
(CWD) mycobacterial forms belonging to M.
tuberculosis complex (over 95%); 2) both phases are
antigenically identical parts of the L-cycle; 3) «round
bodies» of the «infective» phase have an endolysosomal
evolution; 4) uncommon vacuolated forms represent a
labile spheroplast stage; 5) the yeastlike bodies are
specialized sinusoidal large bodies of unknown function.
Results for series B show that in roughly two thirds of
cases the pigmented forms are also CWD mycobacteria,
have the same immunophenotype as sarcoid PCs in
35.7% of cases, have a much higher incidence of labile
vacuolated forms and, finally, that malignancy associated «pseudosarcoid» granulomas do not differ
antigenically from genuine sarcoid granulomas. Unlike
conventional mycobacteria, PCs do not express
cytoskeletal proteins consistently. Their general
reactivity for HBcAg raises the possibility of phage
interactions being responsible for the L-cycle since it
may reflect shared epitopes between unrelated virus
entities.
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