Interleukin (IL)‐17‐producing pathogenic T lymphocytes co‐express CD20 and are depleted by rituximab in primary Sjögren's syndrome: a pilot study

• Published in: Clinical and experimental immunology 2016-06, Vol.184 (3), p.284-292
• Main Authors: Alunno, A., Carubbi, F., Bistoni, O., Caterbi, S., Bartoloni, E., Di Benedetto, P., Cipriani, P., Giacomelli, R., Gerli, R.
• Format: Article
• Language: English
• Subjects: Adrenal Cortex Hormones - therapeutic use; Adult; Antigens, CD20 - genetics; Antigens, CD20 - immunology; CD3 Complex - genetics; CD3 Complex - immunology; CD4 Antigens - genetics; CD4 Antigens - immunology; CD8 Antigens - genetics; CD8 Antigens - immunology; Dexamethasone - analogs & derivatives; Dexamethasone - therapeutic use; Female; Gene Expression; Humans; Immunologic Factors - therapeutic use; Interleukin-17 - genetics; Interleukin-17 - immunology; Middle Aged; Original; Pilot Projects; Primary Cell Culture; rituximab; Rituximab - therapeutic use; salivary glands; Salivary Glands - drug effects; Salivary Glands - immunology; Salivary Glands - pathology; Sjogren's Syndrome - drug therapy; Sjogren's Syndrome - genetics; Sjogren's Syndrome - immunology; Sjogren's Syndrome - pathology; Sjögren's syndrome; Th17 cells; Th17 Cells - drug effects; Th17 Cells - immunology; Th17 Cells - pathology
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/cei.12771

Summary Compelling evidence suggests that interleukin (IL)‐17 and IL‐17‐producing cells play a pivotal role in the pathogenesis of primary Sjögren's syndrome (pSS). We investigated phenotypical and functional effects of the anti‐CD20 antibody rituximab (RTX) on circulating and glandular IL‐17‐producing T cells in pSS. RTX is able to deplete glandular IL‐17+ CD3+CD4–CD8– double‐negative (DN) and CD4+ Th17 cells as well as circulating IL‐17+ DN T cells. A fraction of glandular and circulating IL‐17+ DN cells and CD4+ T helper type 17 (Th17) cells co‐expresses CD20 on the cell surface explaining, at least in part, such depletive capacity of RTX. The exposure to RTX does not rescue the in‐vitro corticosteroid resistance of IL‐17+ DN T cells. Our results support further the therapeutic role in pSS of RTX that, despite its B cell specificity, appears able to also hamper IL‐17‐producing T cells in this disease.