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The Journal of Immunology, Vol 157, Issue 5 1958-1964, Copyright © 1996 by American Association of Immunologists
ARTICLES |
AC Theodore, DM Center, J Nicoll, G Fine, H Kornfeld and WW Cruikshank
The Pulmonary Center, Boston University School of Medicine, MA 02118, USA.
CD4 participation in TCR/CD3-associated activation through interaction with the MHC class II Ags results in formation of a CD4-TCR/CD3 complex capable of maximal signal transduction. When CD4 binds to alternative ligands such as HIV-1 gp120 or anti-CD4 Abs, Ag stimulation of TCR/CD3 is markedly inhibited, and an unresponsive state develops. To determine if the natural CD4 ligand interleukin-16 also induces unresponsiveness, we tested the effects of rIL-16 on T cell proliferation in mixed lymphocyte reactions. rIL-16 suppressed T cell proliferation in a dose- dependent manner at concentrations of 10(-11) to 10(-7) M. Inhibition of proliferation was present on days 5 to 9 of the mixed lymphocyte reaction. rIL-16 did not modulate membrane CD4, significantly change basal [3H]thymidine incorporation in resting T lymphocytes, or alter viability. The suppressive effect was specifically blocked by preincubation with neutralizing anti-rIL-16 mAb or with recombinant soluble CD4. While the expression of IL-2R on responder cells was unaffected by rIL-16, the addition of exogenous rIL-2 did not restore T cell responsiveness. The unresponsiveness induced by rIL-16 is distinct from that of other CD4 ligands in that CD4 and IL-2R expression are unaffected. The failure of rIL-2 to restore proliferation suggests that the decrease in T cell responsiveness induced by rIL-16 may result from an interruption in the IL-2R-signaling mechanism. These results may help explain how CD4 delivers both activating and inhibitory signals and provides a rationale for the role of IL-16 in the regulation of immune responses.
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N. A. Parada, D. M. Center, H. Kornfeld, W. L. Rodriguez, J. Cook, M. Vallen, and W. W. Cruikshank Synergistic Activation of CD4+ T Cells by IL-16 and IL-2 J. Immunol., March 1, 1998; 160(5): 2115 - 2120. [Abstract] [Full Text] [PDF]
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S. Laberge, P. Ernst, O. Ghaffar, W. W. Cruikshank, H. Kornfeld, D. M. Center, and Q. Hamid Increased Expression of Interleukin-16 in Bronchial Mucosa of Subjects with Atopic Asthma Am. J. Respir. Cell Mol. Biol., August 1, 1997; 17(2): 193 - 202. [Abstract] [Full Text]
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Y. Zhang, H. Kornfeld, W. W. Cruikshank, S. Kim, C. C. Reardon, and D. M. Center Nuclear Translocation of the N-terminal Prodomain of Interleukin-16 J. Biol. Chem., January 5, 2001; 276(2): 1299 - 1303. [Abstract] [Full Text] [PDF]
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