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Updated: Aug 18, 2026

Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
A study of accessory cells in the acquired lymphoid tissue of helicobacter gastritis
P Sarsfield1, D B Jones, A C Wotherspoon
1University Department of Pathology, Southampton General Hospital, U.K.
This paper presents a description of the patterns of distribution of accessory cells in helicobacter gastritis and low-grade gastric MALT lymphomas. The use of gastric resection specimens afforded abundant, well-orientated lymphoid tissue. Fifteen cases were selected from patients with MALT lymphomas, three with gastritis alone, and six histologically normal controls. A panel of antibodies working in paraffin-embedded tissue, identifying differing accessory cells, was used. These comprised antibodies to HLA class II (WR18), acid cysteine proteinase inhibitor (ACPI), CD68 (PGM1), Factor XIIIa, S100 protein, CD23 (BU38), CD106 (V-CAM1), CD55 (BRIC 128), and CD21 (1F8). CD68-positive macrophages in the gastritis cases were abundant in the superficial mucosa. Factor XIIIa also identified dendritic cells at deeper sites but these were absent from both the acquired and the neoplastic lymphoid tissue. Antibodies to both S100 protein and ACPI stained dendritic cells localized to areas within and adjacent to the lymphoid tissue only. S100 protein-positive cells were concentrated in close contact with glandular epithelium immediately above the germinal centres, while ACPI-positive dendritic cells were identified, especially around the more blastic reactive follicles, in the intervening space between the germinal centres and the overlying epithelium. Similar patterns of organization were also seen in the areas of mucosal lymphoma. The follicular dendritic markers revealed overlapping but distinct sub-populations within the germinal centres which appeared to alter depending on the activity of the germinal centres. While both ACPI and CD55 stained the germinal centre dendritic reticulum cell networks only, CD21 and CD106 also stained the mantle dendritic cells. The proportion staining with CD23, which stains dendritic reticulum cells within the centrocyte-rich areas of the germinal centres only, was greatest in the more quiescent germinal centres. Similar patterns of staining were also seen in germinal centres within the gastric MALT lymphomas. It is proposed that the sub-populations of dendritic cells staining with S100 protein and ACPI may facilitate helicobacter antigen delivery to the germinal centres. The follicular dendritic cells then promote a sustained B-cell response to the luminal pathogen.
This paper presents a description of the patterns of distribution of accessory cells in helicobacter gastritis and low-grade gastric MALT lymphomas. The use of gastric resection specimens afforded abundant, well-orientated lymphoid tissue. Fifteen cases were selected from patients with MALT lymphomas, three with gastritis alone, and six histologically normal controls. A panel of antibodies working in paraffin-embedded tissue, identifying differing accessory cells, was used. These comprised antibodies to HLA class II (WR18), acid cysteine proteinase inhibitor (ACPI), CD68 (PGM1), Factor XIIIa, S100 protein, CD23 (BU38), CD106 (V-CAM1), CD55 (BRIC 128), and CD21 (1F8). CD68-positive macrophages in the gastritis cases were abundant in the superficial mucosa. Factor XIIIa also identified dendritic cells at deeper sites but these were absent from both the acquired and the neoplastic lymphoid tissue. Antibodies to both S100 protein and ACPI stained dendritic cells localized to areas within and adjacent to the lymphoid tissue only. S100 protein-positive cells were concentrated in close contact with glandular epithelium immediately above the germinal centres, while ACPI-positive dendritic cells were identified, especially around the more blastic reactive follicles, in the intervening space between the germinal centres and the overlying epithelium. Similar patterns of organization were also seen in the areas of mucosal lymphoma. The follicular dendritic markers revealed overlapping but distinct sub-populations within the germinal centres which appeared to alter depending on the activity of the germinal centres. While both ACPI and CD55 stained the germinal centre dendritic reticulum cell networks only, CD21 and CD106 also stained the mantle dendritic cells. The proportion staining with CD23, which stains dendritic reticulum cells within the centrocyte-rich areas of the germinal centres only, was greatest in the more quiescent germinal centres. Similar patterns of staining were also seen in germinal centres within the gastric MALT lymphomas. It is proposed that the sub-populations of dendritic cells staining with S100 protein and ACPI may facilitate helicobacter antigen delivery to the germinal centres. The follicular dendritic cells then promote a sustained B-cell response to the luminal pathogen.
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