The Journal of Immunology, Vol 133, Issue 4 1716-1722, Copyright © 1984 by American Association of Immunologists

ARTICLES

Studies on the mechanism of the enhancement of delayed-type hypersensitivity by pertussigen

WA Sewell, JJ Munoz, R Scollay and MA Vadas

The potentiation of delayed-type hypersensitivity (DTH) reactions by pertussigen, a protein toxin from Bordetella pertussis, has been studied in adoptive transfer assays. Lymph node or spleen cells from mice treated with or without pertussigen at the time of immunization with protein antigens were transferred to naive, syngeneic recipients that were challenged with antigen. Cells from donors treated with pertussigen had the capacity to transfer vigorous, antigen-specific DTH reactions. Cells from immunized donors not given pertussigen transferred little or no DTH. These results indicate that pertussigen is able to augment DTH reactions by potentiating the antigen reactivity of cell populations in lymphoid organs. The phenotype of the effector cells induced by pertussigen was Thy-1 positive, L3T4 positive, and Ly- 2 negative. Cells from mice given pertussigen and an irrelevant antigen had no influence on specific DTH responses, suggesting that pertussigen enhances the activity of the antigen-specific cell type mediating DTH. The effect of pertussigen and of immunization on the lymphocyte subpopulations present in the lymph nodes was studied by analysis of suspensions of lymph node cells by flow cytometry. In immunized and in nonimmune mice, pertussigen increased the ratio of Ly-2-negative:Ly-2- positive T cells, and reduced the overall proportion of B cells. In immunized mice, pertussigen induced a much higher proportion of large dividing cells from 5 days after sensitization onwards. The relevance of these changes in lymphocyte behavior to the development of enhanced and prolonged DTH in mice given pertussigen is discussed.

This article has been cited by other articles:

				R. Noubade, N. Saligrama, K. Spach, R. del Rio, E. P. Blankenhorn, T. Kantidakis, G. Milligan, M. Rincon, and C. Teuscher Autoimmune Disease-Associated Histamine Receptor H1 Alleles Exhibit Differential Protein Trafficking and Cell Surface Expression J. Immunol., June 1, 2008; 180(11): 7471 - 7479. [Abstract] [Full Text] [PDF]

				J. M. Millward, M. Caruso, I. L. Campbell, J. Gauldie, and T. Owens IFN-{gamma}-Induced Chemokines Synergize with Pertussis Toxin to Promote T Cell Entry to the Central Nervous System J. Immunol., June 15, 2007; 178(12): 8175 - 8182. [Abstract] [Full Text] [PDF]

				J. Y. Wu, Y. Jin, R. A. Edwards, Y. Zhang, M. J. Finegold, and M. X. Wu Impaired TGF-{beta} Responses in Peripheral T Cells of G{alpha}i2-/- Mice J. Immunol., May 15, 2005; 174(10): 6122 - 6128. [Abstract] [Full Text] [PDF]

				J. F. Gao, S. B. Call, P. D. Fillmore, T. Watanabe, N. D. Meeker, and C. Teuscher Analysis of the Role of Bphs/Hrh1 in the Genetic Control of Responsiveness to Pertussis Toxin Infect. Immun., March 1, 2003; 71(3): 1281 - 1287. [Abstract] [Full Text] [PDF]

				D. Huang, M. Tani, J. Wang, Y. Han, T. T. He, J. Weaver, I. F. Charo, V. K. Tuohy, B. J. Rollins, and R. M. Ransohoff Pertussis Toxin-Induced Reversible Encephalopathy Dependent on Monocyte Chemoattractant Protein-1 Overexpression in Mice J. Neurosci., December 15, 2002; 22(24): 10633 - 10642. [Abstract] [Full Text] [PDF]

				R. Z. Ma, J. Gao, N. D. Meeker, P. D. Fillmore, K. S. K. Tung, T. Watanabe, J. F. Zachary, H. Offner, E. P. Blankenhorn, and C. Teuscher Identification of Bphs, an Autoimmune Disease Locus, as Histamine Receptor H1 Science, July 26, 2002; 297(5581): 620 - 623. [Abstract] [Full Text] [PDF]

				D. Huang, J. Wang, P. Kivisakk, B. J. Rollins, and R. M. Ransohoff Absence of Monocyte Chemoattractant Protein 1 in Mice Leads to Decreased Local Macrophage Recruitment and Antigen-specific T Helper Cell Type 1 Immune Response in Experimental Autoimmune Encephalomyelitis J. Exp. Med., March 19, 2001; 193(6): 713 - 726. [Abstract] [Full Text] [PDF]