B cell clonality in gastric lymphoid tissues of patients with Sjogren's syndrome

Objective-To determine the prevalence of mucosa associated lymphoid tissue (MALT) in the stomach and of a possible antigen driven proliferation, in patients with Sjogren's syndrome (SS). Methods-Twenty one patients with primary SS and 80 dyspeptic controls underwent upper endoscopy. Lymphoid tissue and Helicobacter pylon were assessed by histopathological analysis. Epstein-Barr virus (EBV) or human herpes virus-6 (HHV-6) genome were studied by polymerase chain reaction (PCR) DNA amplification. Two PCR VDJ procedures were used to detect immunoglobulin heavy chain (IgH) gene rearrangement. Results-Organised MALT was found in 33.3% of the patients, compared with 21P5% of the controls (NS). H pylon infection was seen in 71% of patients and 63% of controls. Genomic EBV or HHV-6 was found in a minor portion ofSS gastric tissues. B celi expansion was detected in nine ofthe 21 patients. Infectious agents in the stomach might have contributed to B celi clonality only in 55.50/0 ofthe cases. No strict relationship was found between lymphoid follicles and clonality. Conclusion-Lymphoid accumulation in the gastric mucosa is common in Sjogren's syndrome, but full evidence for an antigen driven B cell expansion could not be demonstrated. Only a portion of those with clonal B celi expansion had evidence of an infectious agent. Other unknown infectious agents or factors related to the underlying disease (autoantigen) and its tissue environment may have a further role as possible causes of B clonal expansion in the gastric mucosa.