Sarcoidosis is not associated with a generalized defect in T cell suppressor function

C. Saltini, J. R. Spurzem, M. R. Kirby, R. G. Crystal

Research output: Contribution to journalArticle

6 Citations (Scopus)


In pulmonary sarcoidosis, the marked expansion of CD4+ (helper/inducer) T cells in the alveolar structures of the lung is maintained by local IL-2 release by activated CD4+ HLA-DR+ T cells without concomitant expansion and activation of CD8+ (suppressor/cytotoxic) T cells, suggesting that sarcoid may be associated with a generalized abnormality of CD8+ T cells. Consistent with this concept, evaluation of the expression of the IL-2R on fresh lung T cells from individuals with active sarcoidosis demonstrated that 7 ± 1% of sarcoid lung CD4+ T cells are spontaneously expressing the IL-2R compared with only 1 ± 1% lung CD8+ T cells (p < 0.01). However, stimulation of purified sarcoid blood CD8+ T cells with the anti-T3/TCR complex mAb OKT3 was followed by the normal expression of IL-2R (p > 0.1) and proliferation (p > 0.1). In addition, lung sarcoid CD8+ T cells responded to OKT3 similarity to normal lung CD8+ T cells and to autologous blood CD8+ T cells as regards expression of IL-2R (p > 0.1) and proliferation (p > 0.1). Finally, using CD4+ T cells activated with allogenic Ag to induce, in coculture, fresh autologous CD8+ cells to suppress proliferation of fresh autologous CD4+ cells to the same Ag, sarcoid CD8+ T cells suppressed CD4+ cell proliferation in a normal fashion (p > 0.1). These results demonstrate that sarcoid CD8+ (suppressor/cytotoxic) T cells are competent to respond to a proliferation signal normally and can be induced to normally suppress CD4+ T cell proliferation to Ag, suggesting that the expansion of activated CD4+ T cells in pulmonary sarcoidosis is not due to a generalized abnormality of CD8+ T cells or of their suppressor T cell function.

Original languageEnglish
Pages (from-to)1854-1860
Number of pages7
JournalJournal of Immunology
Issue number6
Publication statusPublished - 1 Jan 1988
Externally publishedYes


ASJC Scopus subject areas

  • Immunology

Cite this