Impact of cigarette smoke on T and B cell responsiveness

• Published in: Cellular immunology 2008-01, Vol.253 (1), p.38-44
• Main Authors: Zavitz, Caleb C.J., Gaschler, Gordon J., Robbins, Clinton S., Botelho, Fernando M., Cox, P. Gerard, Stampfli, Martin R.
• Format: Article
• Language: English
• Subjects: Animals; B-Lymphocytes - drug effects; B-Lymphocytes - immunology; Calcium - metabolism; Cell Proliferation - drug effects; Cells, Cultured; Female; Human; Humans; Lung - cytology; Lung - immunology; Lymph Nodes - cytology; Lymph Nodes - immunology; Lymphocyte; Lymphocyte Activation - drug effects; Lymphocyte Activation - immunology; Lymphocyte Subsets - drug effects; Lymphocyte Subsets - immunology; Mice; Mice, Inbred C57BL; Mouse; Rats; Smoke - adverse effects; Smoking; Smoking - immunology; Spleen - cytology; Spleen - immunology; T-Lymphocytes - drug effects; T-Lymphocytes - immunology; Tobacco
• ISSN: 0008-8749; 1090-2163; 1090-2163
• DOI: 10.1016/j.cellimm.2008.04.012

Although its direct effects cannot be discounted, tobacco’s effects on the immune system have been proposed to play a key role in mediating its deleterious health impact. Studies in rats using high levels of smoke exposure have suggested that tobacco smoke exhausts cellular signal transduction cascades, making lymphocytes unresponsive to stimulation. In the present study, we show that purified B or T cells, and total lymphocytes from the lungs, lymph nodes and spleens of smoke-exposed mice fluxed calcium, proliferated, and secreted immunoglobulin or IFN-γ similarly to control mice when stimulated with ligands including anti-IgM, and anti-CD3. Importantly, we recapitulated these findings in PBMCs from human smokers; cells from long-term smokers and never-smokers proliferated equivalently when stimulated ex vivo. Previous reports of lymphocyte unresponsiveness in rats are inconsistent with these findings, and may reflect a phenomenon observed only at levels of smoke exposure well above those seen in actual human smokers.