Oligoclonal expansions of T-cell repertoire in gastric mucosa associated lymphoid tissue type B-cell lymphoma and adjacent gastritis

Citation
W. Haedicke et al., Oligoclonal expansions of T-cell repertoire in gastric mucosa associated lymphoid tissue type B-cell lymphoma and adjacent gastritis, DIAGN MOL P, 8(3), 1999, pp. 138-144
Citations number
36
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
DIAGNOSTIC MOLECULAR PATHOLOGY
ISSN journal
10529551 → ACNP
Volume
8
Issue
3
Year of publication
1999
Pages
138 - 144
Database
ISI
SICI code
1052-9551(199909)8:3<138:OEOTRI>2.0.ZU;2-4
Abstract
Local stimulation by Helicobacter pylori (HP), autoantigen: and a concurren t T-cell-mediated stimulation of B cells are believed to play an important role in gastric mucosa-associated lymphoid tissue (MALT) type B cell lympho magenesis. Many autoimmune diseases have shown to lead to a skewed T-cell r epertoire with autoantigen specific expansions and deletions. Characterizat ion of lymphoma and gastritis areas of seven gastrectomy specimens using a T-cell receptor beta variable chain (TCR beta V) family-specific reverse tr anscriptase (RT)polymerase chain reaction (PCR) assay and fluorescence-acti vated cell sorter (FACS) analysis revealed a local chronic and acute activa tion of T cells in lymphoma and an oligoclonal T-cell repertoire in gastrit is and in lymphoma, partially sharing the same clones. Local activation and a partial identity suggest that an antigenic challenge caused by a common local pathogen may still continue to take place in MALT type lymphoma as in gastritis, consistent with the view that gastritis may be a precursor lesi on of MALT type lymphoma. Expansions that were found only in one of the com partments suggest that also an immune hyperstimulation may contribute to th e T-cell repertoire, possibly because of certain tissue antigens. Deletions of TCR PV families found only in gastritis underline the view that autoant igen may play an important role in its pathogenesis.