T cell genetic background determines default T helper phenotype development in vitro

doi:10.1084/jem.181.2.713

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T cell genetic background determines default T helper phenotype development in vitro

CS Hsieh, SE Macatonia, A O'Garra and KM Murphy
Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110.

A host's ability to resist certain pathogens such as Leishmania major can depend upon the phenotype of T helper (Th) subset that develops. Different murine genetic backgrounds are known to significantly alter the direction of Th subset development, although the cellular basis of this influence is poorly understood. To examine the basis of this effect we used an in vitro alpha/beta-T cell receptor (TCR) transgenic system for analysis of Th phenotype development. To control for TCR usage, we derived the DO11.10 alpha/beta-TCR transgene in several genetic backgrounds. Our findings suggest that the effects of genetic background on Th phenotype development reside within the T cell, and not the antigen-presenting cell compartment. Transgenic T cells from both the B10.D2 and BALB/c backgrounds showed development toward either the Th1 or Th2 phenotype under the strong directing influence of interleukin (IL) 12 and IL4, respectively. However, when T cells were activated in vitro under neutral conditions in which exogenous cytokines were not added, B10.D2-derived T cells acquired a significantly stronger Th1 phenotype than T cells from the BALB/c background, correspondent with in vivo Th responses to Leishmania in these strains. Importantly, these cytokine differences resulted in distinct functional properties, because B10.D2- but not BALB/c-derived T cells could induce macrophage production of nitric oxide, an important antimicrobial factor. Thus, the genetically determined default Th phenotype development observed in vitro may correspond to in vivo Th subset responses for pathogens such as Leishmania which do not initiate strong Th phenotype-directing signals.
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Maecker, H. T., Do, M.-S., Levy, S. (1998). CD81 on B cells promotes interleukin 4�secretion and antibody production during T helper type 2�immune�responses. Proc. Natl. Acad. Sci. USA 95: 2458-2462 [Abstract] [Full Text]
Shibuya, K., Robinson, D., Zonin, F., Hartley, S. B., Macatonia, S. E., Somoza, C., Hunter, C. A., Murphy, K. M., O'Garra, A. (1998). IL-1{alpha} and TNF-{alpha} Are Required for IL-12-Induced Development of Th1 Cells Producing High Levels of IFN-{gamma} in BALB/c But Not C57BL/6 Mice. J. Immunol. 160: 1708-1716 [Abstract] [Full Text]
Reiner, S. L., Fowell, D. J., Moskowitz, N. H., Swier, K., Brown, D. R., Brown, C. R., Turck, C. W., Scott2, P. A., Killeen, N., Locksley3, R. M. (1998). Control of Leishmania major by a Monoclonal {alpha}{beta} T Cell Repertoire. J. Immunol. 160: 884-889 [Abstract] [Full Text]
Gross, D. M., Steere, A. C., Huber, B. T. (1998). T Helper 1 Response Is Dominant and Localized to the Synovial Fluid in Patients with Lyme Arthritis. J. Immunol. 160: 1022-1028 [Abstract] [Full Text]
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Pearson, C.I., van Ewijk, W., McDevitt, H.O. (1997). Induction of Apoptosis and T Helper 2�(Th2) Responses Correlates with Peptide Affinity for the Major Histocompatibility Complex in Self-reactive T Cell Receptor Transgenic Mice. J. Exp. Med. 185: 583-600 [Abstract] [Full Text]
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