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Clinical and Experimental Immunology logoLink to Clinical and Experimental Immunology
. 1977 Oct;30(1):89–96.

Cell-mediated immunity in systemic lupus erythematosus

A A Andrianakos, P N Tsichlis, E G Merikas, S G Marketos, J T Sharp, G E Merikas
PMCID: PMC1541176  PMID: 606439

Abstract

Cell-mediated immunity in systemic lupus erythematosus (SLE) was assessed by skin testing with six common antigens and by streptokinase-streptodornase (SK–SD) induced leucocyte migration inhibition in twenty-four SLE patients, who were age- and sex-matched with twenty-four healthy subjects or patients with diseases not known to be associated with immunological abnormalities. 25% of SLE patients were anergic, and the migration of their leucocytes was not inhibited in the presence of SK–SD. Depressed cell-mediated immune responses were significantly related to disease activity. Patients with inactive or mildly active SLE exhibited selective hyporeactivity to purified protein derivative (PPD), while those with moderately to severely active SLE had marked depression of cell-mediated immunity, as manifested by both skin testing with common antigens and leucocyte migration inhibition in response to stimulation by SK–SD. A significant positive correlation was found between absolute peripheral lymphocyte counts of the SLE patients and the number of their positive skin tests. Peripheral lymphocyte counts were significantly decreased in the anergic SLE patients and in those with moderate to severe disease activity. The correlation found between skin test reactivity and absolute lymphocyte count suggests lymphocytopenia as the mechanism of the immune suppression. On the other hand, lymphocytopenia alone cannot explain the depression of the leucocyte migration inhibition response to SK–SD observed in the SLE patients, because in this system a relatively constant number of lymphocytes is employed. In conclusion, the depression of cell-mediated immune responses in SLE is caused by both lymphocytopenia and lymphocyte hyporeactivity.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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