Expansion of Circulating γδ T Cells in Active Sarcoidosis Closely Correlates with Defects in Cellular Immunity

• Published in: Clinical Immunology and Immunopathology Vol. 74; no. 3; pp. 217 - 222
• Main Authors: Nakata, Koh, Sugie, Takumi, Cohen, Henry, Nakano, Hiroyasu, Aoki, Masakazu
• Format: Book Review Journal Article
• Language: English
• Published: San Diego, CA Elsevier Inc 1995; New York, NY Academic Press; Boston
• Subjects: Biological and medical sciences; Medical sciences; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; Human; Immunosuppression; Sarcoidosis; Pathogenesis; γ/δ T cell receptor; Systemic disease; T-Lymphocyte; Cellular immunity; Cell subpopulation
• ISSN: 0090-1229; 1090-2341
• DOI: 10.1006/clin.1995.1032

The relationship between the level of γδ T cells and cellular immunity oft lymphocytes was assessed in the peripheral blood of active sarcoidosis patients and healthy controls. We divided the active sarcoidosis patients into two groups: a group of patients with a normal distribution of circulating γδ T cells (group A; n = 11, less than 8.2% lymphocytes) and another group with increased γδ T cell levels (group B; n = 11, greater than 8.2% lymphocytes). The proportion and absolute count of CD4 + lymphocytes in group B (28.6 ± 11.2%, 374.1 ± 193.8/μl) were remarkably smaller than control subjects (45.7 ± 6.8%, 818.3 ± 290.2/μl, P < 0.001, P < 0.002, respectively). Group A, however, showed a moderate reduction in CD4 + lymphocytes when compared with controls. Serial measurements of T cell subtypes were performed on five patients in group B. γδ T cells and CD4 + lymphocytes were inversely correlated over the observation period which ranged from 2 to 18 months. When peripheral blood T cells were stimulated with PHA or PPD in vitro, the responses were weaker in group B compared with both group A and control subjects. These results suggest that the increase in circulating γδ T cells in sarcoidosis closely relates to a defect in cellular immunity which progresses during the disease process.