Immunohistologic analysis of lymphoid infiltrates in primary Sjogren's syndrome using monoclonal antibodies.

TC Adamson 3rd, RI Fox, DM Frisman… - Journal of immunology …, 1983 - journals.aai.org
TC Adamson 3rd, RI Fox, DM Frisman, FV Howell
Journal of immunology (Baltimore, Md.: 1950), 1983journals.aai.org
The characterization of lymphocytes infiltrating salivary glands in patients with primary
Sjogren's syndrome (1 degree SS) yields insights to disease pathogenesis that are not
revealed by studies of the corresponding peripheral blood lymphocytes (PBL) alone. We
analyzed salivary gland lymphocytes (SGL) and PBL in 14 patients with untreated 1 degree
SS using monoclonal antibodies that detect T cells, T cell subsets, B cells, and antigens
associated with lymphocyte activation. A four-step biotin-avidin immunoperoxidase …
Abstract
The characterization of lymphocytes infiltrating salivary glands in patients with primary Sjogren's syndrome (1 degree SS) yields insights to disease pathogenesis that are not revealed by studies of the corresponding peripheral blood lymphocytes (PBL) alone. We analyzed salivary gland lymphocytes (SGL) and PBL in 14 patients with untreated 1 degree SS using monoclonal antibodies that detect T cells, T cell subsets, B cells, and antigens associated with lymphocyte activation. A four-step biotin-avidin immunoperoxidase technique was used for salivary gland frozen sections; cell suspensions and PBL were stained cytofluorographically. A predominance of T cells (Leu 1 = L17F12; Leu 4 = OKT3) was found in SGL (greater than 75%) and PBL (76 +/- 9%) with the majority belonging to the Leu 3a (OKT4) subset. A minority of B cells (anti-delta, -kappa, -lambda) was present in both SGL and PBL; however, a subset of B cells defined by monoclonal antibody B532 was present in SGL (5 to 20%) but was absent from PBL. An increased prevalence of activation antigens (Ia; OKT10) was found on SGL T cells (greater than 50% positive) compared to PBL T cells (less than 15% positive). These studies demonstrate that specific antigenic markers on lymphocytes at the site of inflammation in 1 degree SS differ significantly from those of the corresponding PBL. These differences emphasize that theories of disease pathogenesis of 1 degree SS must include studies on SGL.
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