Abstract
The fact that T cells can differentiate and become polarized to produce a certain limited spectrum of cytokines and mediate only a subset of potential T cell functions during cell-cell interactions continues to be an area of intense investigation. The mechanisms by which T-helper (Th) cels mobilize various effector reactions remained unclear until 1986 when Mosmann and Coffman started a conceptual revolution in immunology by dividing murine T cell clones, or Th cells, into the now familiar two subpopulations, Th1 and Th2 based on their restricted and stereotyped profile of cytokine secretion.1 These same two subsets can be generated from ex vivo populations when cultured under appropriate conditions;2 they can also be recovered from immunized animals3 and from patients suffering from a variety of diseases.4.
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Zedler, S., Faist, E. (2000). Pathophysiologic and Clinical Importance of Stress-Induced Th1/Th2 T Cell Shifts. In: Baue, A.E., Faist, E., Fry, D.E. (eds) Multiple Organ Failure. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-1222-5_52
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DOI: https://doi.org/10.1007/978-1-4612-1222-5_52
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