title: Immunolocalization of cell-wall-deficient forms of Mycobacterium tuberculosis complex in sarcoidosis and in sinus histiocytosis of lymph nodes draining carcinoma.
abstract: In sarcoidosis, pleomorphic chromogens (PCs) occur as multivariate pigmented elements within sinusoids of lymph nodes (sinusoidal phase) and as tiny "round bodies" 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 all 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-I-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-wall-deficient (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.
authors.affiliation: Department of Pathology, Harlem Hospital Division, College of Physicians and Surgeons, Columbia University, New York, USA.
authors.forename: H A
authors.initials: HA
authors.lastname: Alavi
authors.forename: E A
authors.initials: EA
authors.lastname: Moscovic
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000737:chemistry; D000911:Antibodies, Monoclonal / Q000737:chemistry; D000918:Antibody Specificity; D002277:Carcinoma / Q000382:microbiology* / Q000473:pathology; D002473:Cell Wall / Q000648:ultrastructure*; D003598:Cytoskeletal Proteins / Q000378:metabolism / Q000648:ultrastructure; D005260:Female; D015618:Histiocytosis, Sinus / Q000382:microbiology* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008175:Lung Neoplasms / Q000382:microbiology* / Q000473:pathology; D008198:Lymph Nodes / Q000382:microbiology* / Q000473:pathology; D008247:Lysosomes / Q000378:metabolism / Q000648:ultrastructure; D008297:Male; D008875:Middle Aged; D009169:Mycobacterium tuberculosis / Q000648:ultrastructure*; D016612:Paraffin Embedding; D010641:Phenotype; D017565:Sarcoidosis, Pulmonary / Q000382:microbiology* / Q000473:pathology
chemical_list: D000907:Antibodies, Bacterial; D000911:Antibodies, Monoclonal; D003598:Cytoskeletal Proteins