
Telocytes in minor salivary glands of primary Sjögren's syndrome: association with the extent of inflammation and ectopic lymphoid neogenesis
Author(s) -
Alunno Alessia,
IbbaManneschi Lidia,
Bistoni Onelia,
Rosa Irene,
Caterbi Sara,
Gerli Roberto,
Manetti Mirko
Publication year - 2015
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12545
Subject(s) - pathology , biology , immunoperoxidase , inflammation , immunohistochemistry , medicine , immunology , antibody , monoclonal antibody
It has been recently reported that telocytes, a stromal (interstitial) cell subset involved in the control of local tissue homeostasis, are hampered in the target organs of inflammatory/autoimmune disorders. Since no data concerning telocytes in minor salivary glands ( MSG s) are currently available, aim of the study was to evaluate telocyte distribution in MSG s with normal architecture, non‐specific chronic sialadenitis ( NSCS ) and primary Sjögren's syndrome ( pSS )‐focal lymphocytic sialadenitis. Twelve patients with pSS and 16 sicca non‐ pSS subjects were enrolled in the study. MSG s were evaluated by haematoxylin and eosin staining and immunofluorescence for CD 3/ CD 20 and CD 21 to assess focus score, Tarpley biopsy score, T/B cell segregation and germinal center ( GC )‐like structures. Telocytes were identified by immunoperoxidase‐based immunohistochemistry for CD 34 and CD 34/platelet‐derived growth factor receptor α double immunofluorescence. Telocytes were numerous in the stromal compartment of normal MSG s, where their long cytoplasmic processes surrounded vessels and encircled both the excretory ducts and the secretory units. In NSCS , despite the presence of a certain degree of inflammation, telocytes were normally represented. Conversely, telocytes were markedly reduced in MSG s from pSS patients compared to normal and NSCS MSG s. Such a decrease was associated with both worsening of glandular inflammation and progression of ectopic lymphoid neogenesis, periductal telocytes being reduced in the presence of smaller inflammatory foci and completely absent in the presence of GC ‐like structures. Our findings suggest that a loss of MSG telocytes might have important pathophysiological implications in pSS . The specific pro‐inflammatory cytokine milieu of pSS MSG s might be one of the causes of telocyte loss.