Primary Sjögren's syndrome (SS) is considered a benign autoimmune disease; it is characterized by lymphoid infiltration of salivary and lacrimal glands, often accompanied by the presence of serum autoantibodies, particularly anti‐Ro (SS‐A) and anti‐La (SS‐B). There are important immunologic similarities between primary SS and acquired immunodeficiency syndrome. To investigate for a possible immune response to retroviral proteins in primary SS, we performed immunoblotting against human immunodeficiency virus‐1 (HIV‐1) proteins using sera from 47 patients with primary SS. Moderate‐to‐strong reactivity, suggesting the presence of serum antibodies, was found in 14 patients (30%). Of 120 normal subjects, only 1 showed moderate positivity. All 14 positive SS sera reacted against p24 (gag) but failed to react against gp41 or gp120 (env). This response did not reflect hypergammaglobulinemia since immunoglobulin concentrations among the 29 SS patients studied were the same in sera that contained and sera that did not contain anti‐gag reactivity. Two sera also reacted against p17 gag. Four reacted against HIV‐2 core proteins, but none reacted with core proteins of human T lymphotropic virus‐I. Only 1 of the 14 sera reacted against Ro (SS‐A), and 1 other reacted against La (SS‐B). These results identify a subset of SS patients characterized by 1) the presence of serum antibodies to HIV‐1 group‐specific, but not type‐specific, proteins, and 2) the relative absence of anti‐Ro (SS‐A) and anti‐La (SS‐B) autoantibodies. In this latter respect, these SS patients constitute a subpopulation that resembles patients with HIV‐induced SS‐like disease.

In this investigation of B cells expressing the CD5 (Leu-1) cell surface marker, we found increased numbers of these cells in 13 of 19 patients with primary Sjiigren's syndrome (SS) (68%), as well as in the rheumatoid arthritis patients. The percentage of B cells that demonstrated increased expression of CD5 was 46% in SS patients, 47% in rheumatoid arthritis patients, 24% in systemic lupus erythematosus patients, and 26% in normal subjects. Over a 2-year period, CD5 expression on B cells was a stable finding in several patients, except for 2 who required either steroid therapy or combined chemotherapy and irradiation for malignant lymphoma. Both of these patients had clinical remissions and their levels of CD5+ B cells returned to normal. The first patient had a clinical picture of SS/systemic lupus erythematosus overlap, associated with polyclonal B cell activation and decreased production of interleukin-2 in response to stimulation with phytohemagglutinin. These cellular immune abnormalities returned to normal after the institution of corticosteroids. Our observations suggest a rela-