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

Alunno A. | Zendy; Carubbi F. | Zendy; Bistoni O. | Zendy; Caterbi S. | Zendy; Bartoloni E. | Zendy; Di Benedetto P. | Zendy; Cipriani P. | Zendy; Giacomelli R. | Zendy; Gerli R. | Zendy

Open Access

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

Author(s) -

Alunno A.,

Carubbi F.,

Bistoni O.,

Caterbi S.,

Bartoloni E.,

Di Benedetto P.,

Cipriani P.,

Giacomelli R.,

Gerli R.

Publication year - 2016

Publication title -

clinical & experimental immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.329

H-Index - 135

eISSN - 1365-2249

pISSN - 0009-9104

DOI - 10.1111/cei.12771

Subject(s) - cd20 , immunology , rituximab , cd8 , interleukin 17 , interleukin 21 , pathogenesis , antibody , interleukin , cd3 , cytotoxic t cell , medicine , biology , cytokine , antigen , in vitro , biochemistry

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.

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