Lymphocyte apoptosis in adult and juvenile systemic lupus erythematosus : relationship with disease activity and lymphopenia

Abstract EN

Background: Systemic lupus erythematosus (SLE) is a heterogeneous and complex group of disorders of uncertain cause.

Recent studies have suggested that abnormalities in the apoptotic cell death may play an important role in the initiation and progression of this disease by altering the generation and cleavage of antigens, and through abnormalities in immuno-regulation.

Objectives: To clarify the extent of apoptotic peripheral blood lymphocytes in adult and juvenile SLE and to determine their relationship with disease activity and lymphopenia.

Methods: Peripheral blood lymphocyte apoptosis in 32 female SLE patients [group I (G1) 16 adult SLE & group II (G2) 16 juvenile SLE] and 32 healthy female volunteers [group III (G3) 16 adult females & group IV (G4) 16 female children] was assessed with flowcytometry.

Results: The percentage of apoptotic lymphocytes was increased in the peripheral blood (PB) of both adult and juvenile SLE patients as compared with their relevant controls (p<0.001).

Peripheral blood lymphocyte apoptosis showed an insignificant relationship with all clinical parameters of disease activity except photosensitivity, which was associated with increased PB lymphocyte apoptosis (p<0.01) in patients’ groups.

PB lymphocyte apoptosis correlated positively with anti ds-DNA (p < 0.01 in G1and p < 0.05 in G2) and negatively with C3c (p < 0.05 in both G1 and G2) and lymphocytic count (p < 0.01 in G1 and p < 0.05 in G2).

Conclusion: The percentage of lymphocyte apoptosis is significantly elevated in both adult and juvenile SLE.

It relates with photosensitivity and correlates with some of the standard parameters of disease activity.

This keeps the process of apoptosis at the center of pathogenetic interest in the generation of autoantibodies.

Targeting such a possible pivotal mechanism might have a favourable impact on the management of such patients.

In the same context it might rationalize the suggested autocrine suicide as a possible mechanism in mediating SLE associated lymphopenia.