Peripheral Blood Lymphocyte Cell Surface Markers during the Course of Systemic Lupus Erythematosus

136

One hundred fifty-eight patients with active, untreated systemic lupus erythematosus (SLE) were studied from the time of diagnosis. Lymphopenia was present in 75%, and another 18% of these patients developed lymphopenia subsequent to disease reactivation. Lymphopenia of less than 1500 cells/pl occurred more frequently than any of the preliminary criteria for the classification of SLE, and it was the most prevalent initial laboratory abnormality. Lymphocyte counts were significantly lower in lupus than in the other connective tissue diseases except mixed connective tissue disease and polymyositis.It has been well recognized that immunological mechanisms are implicated in the pathogenesis of systemic lupus erythematosus (SLE). Although lymphocytes play a paramount role in the immune response (1,2),

Section: Discussionmentioning

confidence: 85%

Lymphopenia In Systemic Lupus Erythematosus

Rivero

Díaz-Jouanen

Alarcón‐Segovia

1978

136

“…I t is therefore possible that alterations in lymphocyte membranes or even virally coded membrane antigens are responsible for producing antibodies that cross-react with similar determinants in a heterogeneous panel of normal test lymphocytes. N o evidence for specific lupusrelated antigens has yet been produced, despite repeated attempts to demonstrate such specificity (6,7,9,41). A recent report by Lewis et a1 (42) might be interpreted as evidence for possible viral antigens detectable in peripheral blood lymphoid cells of patients with active SLE.…”

Section: Discussionmentioning

confidence: 99%

IgG antilymphocyte antibodies in SLE detected by ¹²⁵I protein A

Williams

Bankhurst

Montano

1976

Self Cite

“…Fluorescein isothiocyanate (FITC) conjugated goat antiserum to h u m a n IgG, IgA, and IgM was obtained f r o m Hyland Laboratories (FITC-Anti-Ig). Monospecific rabbit anti-IgG, IgA, and IgM sera were prepared on immunoabsorbent columns and labeled with FITC as previously described (1).…”

Section: Methodsmentioning

confidence: 99%

“…is increased (1)(2)(3). T h e percent of cells bearing a second B-lymphocyte marker, the receptor for the third component of complement, is decreased (1).…”

mentioning

confidence: 99%

Antilymphocyte antibodies in systemic lupus erythematosus

Messner

Kennedy

Jelinek

1975

Self Cite

Antilymphocyte antibodies in SLE bind to normal lymphocytes and are not always associated with lymphocytotoxic activity. Detection of these antibodies on the surface of normal lymphocytes by immunofluorescent techniques is enhanced by short incubation periods, reduced temperature, and metabolic inhibition. T h e same effects occur in SLE blood and may influence the enumeration of B lymphocytes as determined by surface immunoglobulin. The percent of T lymphocytes forming sheep erythrocyte rosettes is not affected by these antibodies.Recent efforts to determine abnormalities in thymic (T) and bone marrow dependent (B) is increased (1-3). T h e percent of cells bearing a second B-lymphocyte marker, the receptor for the third component of complement, is decreased (1). T lymphocytes as determined by anti-T-cell serum or by rosette formation with sheep erythrocytes (E rosettes) are also decreased in SLE (1,2,4-6). Other work has demonstrated that antibodies reactive with lymphocytes (7,8), and in particular with T lymphocytes (6,9), are found in many of these patients. It is thus possible that the apparent alteration in percent T and B lymphocytes in SLE might be due to adherence of antilymphocyte antibodies to the surface of T cells. Initial attempts to demonstrate attachment of SLE antilymphocyte antibodies to normal lymphocytes by fluorescent techniques were relatively unsuccessful (1). T h e present study was undertaken to determine whether alterations in experimental conditions might allow the detection of these antibodies, and to gain more information about their effect on lymphocyte surface characteristics. MATERIALS AND METHODSLymphocytes were obtained from healthy men and women aged 20 t o 38 years and patients with systemic l u p u s erythematosus (SLE). Each patient met the criteria for the diagnosis of S L E established by the American Rheumatism Association (10). Lymphocytes were isolated from whole heparinized blood using differential centrifugatian as described previously (1 l). Fluorescein isothiocyanate (FITC) conjugated goat antiserum to h u m a n IgG, IgA, and IgM was obtained f r o m Hyland Laboratories (FITC-