Publication | Open Access
Immunohistologic analysis of lymphoid infiltrates in primary Sjogren's syndrome using monoclonal antibodies.
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1983
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Clinical ImmunologyCorresponding PblImmunologyImmune RegulationPathologyImmune SystemImmunotherapyInflammationRheumatologyAutoimmune DiseaseSalivary GlandsAutoimmunityImmunologic DiseaseSclerodermaPrimary SjogrenPbl T CellsSjögren’s SyndromeLymphoid InfiltratesMonoclonal AntibodiesMedicineImmunological Biomarkers
Lymphocyte infiltration of salivary glands in primary Sjogren’s syndrome provides pathogenesis insights that peripheral blood studies miss. The study examined salivary gland and peripheral blood lymphocytes from 14 untreated patients using monoclonal antibodies against T‑cell subsets, B cells, and activation markers, applying a four‑step biotin‑avidin immunoperoxidase protocol to frozen gland sections and cytofluorographic staining of cell suspensions. T cells dominated both glandular (over 75 %) and peripheral (76 ± 9 %) populations, mainly the Leu3a subset, while B cells were scarce; a B532‑positive subset appeared only in glands, and activation antigen expression was >50 % on glandular T cells versus <15 % in blood, underscoring distinct local immune profiles that must be considered in disease pathogenesis.
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.