IDENTIFICATION OF HUMAN THYMIC EPITHELIAL CELLS WITH ANTIBODIES TO THYMOSIN ?1, IN MYASTHENIA GRAVIS

1981 ◽  
Vol 377 (1 Myasthenia Gr) ◽  
pp. 477-485 ◽  
Author(s):  
Marinos C. Dalakas ◽  
W. King Engel ◽  
John E. McClure ◽  
Allan L. Goldstein ◽  
Valerie Askanas
Keyword(s):  
Epithelial Cells ◽  
Myasthenia Gravis ◽  
Thymic Epithelial Cells

scholarly journals A Striational Muscle Antigen and Myasthenia Gravis-Associated Thymomas Share an Acetylcholine-Receptor Epitope

1992 ◽  
Vol 2 (2) ◽  
pp. 77-84 ◽  
Author(s):  
Alexander Marx ◽  
Mary Osborn ◽  
Socrates Tzartos ◽  
Kerstin I. Geuder ◽  
Berthold Schalke ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Myasthenia Gravis ◽  
Acetylcholine Receptor ◽  
Tumor Antigens ◽  
Molecular Mimicry ◽  
Thymic Epithelial Cells ◽  
Characteristic Finding ◽  
The Common ◽  
Secondary Phenomenon ◽  
Type Ii Fibers

The coincidence of autoantibodies against the acetylcholine receptor (AChR) and muscle striational antigens (SA) is a characteristic finding in thymoma-associated myasthenia gravis (MG), but their origins are still unresolved. Some common muscle antigens that were shown to be targets of anti-SA autoantibodies in thymoma-associated MG have also been detected in normal or neoplastic thymic epithelial cells, suggesting that the release of (eventually altered) antigens from the thymic tumors could elicit SA autoimmunity. In contrast to this model, we report here that titin, which is a recently reported target of SA autoimmunity, is not expressed in thymomas. In addition, we show that skeletal muscle type-II fibers exhibit a striational immunoreactivity with monoclonal antibody mAb155, which was previously identified to label a very immunogenic cytoplasmic epitope of the AChR and neoplastic epithelial cells of MGassociated thymomas. We conclude from these findings that titin autoimmunity in thymoma-associated MG is either due to a molecular mimicry mechanism involving tumor antigens (other than titin) or is a secondary phenomenon following release of titin from muscle. Based on the common immunoreactivity of the AChR, a striational antigen and thymoma, we suggest as the pathogenetic mechanism of thymoma-associated MGa "circulus vitiosus" in which SA autoimmunity could help maintain the AChR autoimmunity that is primarily elicited by the thymomas.

scholarly journals Thymic B lymphocyte clones from patients with myasthenia gravis secrete monoclonal striational autoantibodies reacting with myosin, alpha actinin, or actin.

1986 ◽  
Vol 164 (4) ◽  
pp. 1043-1059 ◽  
Author(s):  
C L Williams ◽  
V A Lennon
Keyword(s):  
Skeletal Muscle ◽  
Epithelial Cells ◽  
Myasthenia Gravis ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
B Lymphocyte ◽  
High Yield ◽  
Thymic Epithelial Cells ◽  
Anchoring Proteins ◽  
Mucosal Cells

Striational autoantibodies (StrAb), which react with elements of skeletal muscle cross-striations, occur frequently in patients with thymoma associated with myasthenia gravis (MG). Dissociated thymic lymphocytes from 22 of 72 MG patients secreted StrAb when cultured with PWM. A high yield of EBV-transformed B cell lines was established from thymus, thymoma, and peripheral blood of seven patients with MG, but clones secreting StrAb arose only from the three patients who had StrAb in their sera. The monoclonal StrAb bound to A bands or I bands in skeletal muscle of human, rat, and frog. One bound to mitochondria in addition to myofibrillar I bands. None bound to nuclei, smooth muscle, or gastric mucosal cells. In immunoblot analyses and ELISAs the monoclonal StrAb bound to muscle and nonmuscle isotypes of myosin, alpha actinin, and/or actin. All bound to contractile proteins common to thymus and muscle, and one selectively immunostained epithelial cells of the thymic medulla. From these antigenic specificities we suggest that StrAb might arise as an immune response directed against the cytoskeletal anchoring proteins associated with nicotinic acetylcholine receptors in thymic epithelial cells undergoing neoplastic transformation to thymoma.

Functional Difference between Cortical and Medullar Thymic Epithelial Cells in Patients with Myasthenia Gravis

1987 ◽  
Vol 496 (1 Neuroimmune I) ◽  
pp. 707-710 ◽  
Author(s):  
SLOBODAN APOSTOLSKI ◽  
JELENA GOSPAVIĆ ◽  
KATARINA ISAKOVIĆ ◽  
MILEVA MIĆIĆ ◽  
LJILJANA POPESKOVIĆ ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Myasthenia Gravis ◽  
Thymic Epithelial Cells ◽  
Functional Difference

Thymic epithelial cells of human patients affected by myasthenia gravis overexpress IGF-I immunoreactivity

Apmis ◽  
2008 ◽  
Vol 116 (1) ◽  
pp. 50-58 ◽  
Author(s):  
TSVETANA T. MARINOVA ◽  
STEFANIE KUERTEN ◽  
DANAIL B. PETROV ◽  
DOYCHIN N. ANGELOV
Keyword(s):  
Epithelial Cells ◽  
Myasthenia Gravis ◽  
Thymic Epithelial Cells ◽  
Igf I

scholarly journals Comparative Analysis of Thymic and Blood Treg in Myasthenia Gravis: Thymic Epithelial Cells Contribute to Thymic Immunoregulatory Defects

2020 ◽  
Vol 11 ◽  
Author(s):  
Frédérique Truffault ◽  
Dani Nazzal ◽  
Julien Verdier ◽  
Angeline Gradolatto ◽  
Elie Fadel ◽  
...  
Keyword(s):  
Comparative Analysis ◽  
Epithelial Cells ◽  
Myasthenia Gravis ◽  
Thymic Epithelial Cells

Antibodies to thymic epithelial cells in myasthenia gravis

1991 ◽  
Vol 35 (1-3) ◽  
pp. 101-110 ◽  
Author(s):  
Didier Safar ◽  
Christine Aimé ◽  
Sylvia Cohen-Kaminsky ◽  
Sonia Berrih-Aknin
Keyword(s):  
Epithelial Cells ◽  
Myasthenia Gravis ◽  
Thymic Epithelial Cells

Galectin-1 is expressed by thymic epithelial cells in myasthenia gravis

1996 ◽  
Vol 13 (4) ◽  
pp. 591-597 ◽  
Author(s):  
Charlene Hafer-Macko ◽  
Mabel Pang ◽  
Jeffrey J. Seilhamer ◽  
Linda G. Baum
Keyword(s):  
Epithelial Cells ◽  
Myasthenia Gravis ◽  
Thymic Epithelial Cells

scholarly journals Myasthenia gravis-specific aberrant neuromuscular gene expression by medullary thymic epithelial cells in thymoma

2021 ◽  
Author(s):  
Yoshiaki Yasumizu ◽  
Naganari Ohkura ◽  
Hisashi Murata ◽  
Makoto Kinoshita ◽  
Soichiro Funaki ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Myasthenia Gravis ◽  
Interaction Analysis ◽  
Ectopic Expression ◽  
Cell Interaction ◽  
Thymic Epithelial Cells ◽  
Autoantibody Production ◽  
Dendritic Cell Migration ◽  
Associated Proteins ◽  
Medullary Thymic Epithelial Cells

Myasthenia gravis (MG) is a neurological disease caused by autoantibodies against neuromuscular-associated proteins. While MG is frequently developed in thymoma patients, the etiologic factors for MG are not well understood. Here, by constructing a comprehensive atlas of thymoma using bulk and single-cell RNA-seq, we identified ectopic expression of neuromuscular molecules in MG-associated thymoma (MG-thymoma). These molecules were originated from a distinct subpopulation of medullary thymic epithelial cells (mTECs), which we named neuromuscular mTECs (nmTECs). MG-thymoma also exhibited microenvironments dedicated to autoantibody production, including ectopic germinal center formation, T follicular helper cell accumulation, and type 2 conventional dendritic cell migration. Cell-cell interaction analysis also predicted the interaction between nmTECs and T/B cells via CXCL12-CXCR4. The enrichment of nmTECs presenting neuromuscular molecules within MG-thymoma was further confirmed by immunohistochemically and by cellular composition estimation from MG-thymoma transcriptome. Altogether, this study suggests that nmTECs play a significant role in MG pathogenesis via ectopic expression of neuromuscular molecules.

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