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. 1980 Dec 1;152(6):1554–1562. doi: 10.1084/jem.152.6.1554

Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. VI. Evidence for different T cell receptors in cells that mediate H-21- restricted and H-2D-restricted cutaneous sensitivity responses

PMCID: PMC2186013  PMID: 6969772

Abstract

We have previously shown that cross-reactive sensitivity (CS) responses induced by 4-hydroxy-3-nitrophenyl acetyl-O-succinimide (NP-O-Su) and elicited by its 5-iodo analogue, 4-hydroxy-5-iodo-3-nitrophenyl acetyl- O-succinimide were observed in strains of mice possessing the Igh-1b allotype, but not in strains bearing allotypes Igh-1c or Igh-1j. These CS responses are mediated by T cells and can be transferred to naive recipients that are homologous at either the H-2K, H-2I, or H-2D regions of the major histocompatibility complex. We now extend our analysis of cross-reactive 4-hydroxy-3-nitrophenyl-acetyl (NP)-induced CS responses to inbred strains of mice expressing additional Igh-1 allotypes. In contrast to NP-induced delayed-type hypersensitivity responses, which only display 4-hydroxy-5-iodo-3-nitrophenyl acetyl (NIP) cross-reactivity in Igh-1b-bearing mice, cross-reactive CS responses can also be elicited in NP-primed mice carrying the Igh-1d, Igh-1e, or Igh-1f allotypes. Moreover, cross-reactive NP-induced CS responses could be transferred by NP-O-Su-primed lymph node cells from the AKR (Igh-1d) strain, into naive recipients homologous at the H-2D region, but only non-cross-reactive NP responses could be transferred into strains homologous at the H-2I region. Furthermore, the lack of cross-reactivity in the Igh-1j-bearing C3H strain was not the result of an inability of these mice to recognize NP in association with H-2K/D products, because NP-O-Su-primed cells from C3H donors transferred NP- specific CS responses into both H-2D and H02I homologous recipients. The results are discussed with respect to the nature of the T cell receptors that control NP responses.

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Selected References

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  1. Andó I., Kisielow P. Fine specificity of cytotoxic T lymphocytes: C57BL effector cells induced by autologous cells modified with hapten (4-hydroxy-3-nitro-phenyl)acetyl (NIP) are not heteroclitic. Eur J Immunol. 1979 Mar;9(3):211–213. doi: 10.1002/eji.1830090308. [DOI] [PubMed] [Google Scholar]
  2. Asherson G. L., Ptak W. Contact and delayed hypersensitivity in the mouse. I. Active sensitization and passive transfer. Immunology. 1968 Sep;15(3):405–416. [PMC free article] [PubMed] [Google Scholar]
  3. Binz H., Frischknecht H., Shen F. W., Wigzell H. Idiotypic determinants on T-cell subpopulations. J Exp Med. 1979 Apr 1;149(4):910–922. doi: 10.1084/jem.149.4.910. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Cohen S., McCluskey R. T., Benacerraf B. Studies on the specificity of the cellular infiltrate of delayed hypersensitivity reactions. J Immunol. 1967 Feb;98(2):269–273. [PubMed] [Google Scholar]
  5. Cramer M., Krawinkel U., Melchers I., Imanishi-Kari T., Ben-Neriah Y., Givol D., Rajewsky K. Isolated hapten-binding receptors of sensitized lymphocytes. IV. Expression of immunoglobulin variable regions in (4-hydroxy-3-nitrophenyl) acetyl (NP)-specific receptors isolated from murine B and T lymphocytes. Eur J Immunol. 1979 Apr;9(4):332–338. doi: 10.1002/eji.1830090415. [DOI] [PubMed] [Google Scholar]
  6. Dennert G., Hatlen L. E. Are contact hypersensitivity cells cytotoxic? Nature. 1975 Oct 9;257(5526):486–488. doi: 10.1038/257486a0. [DOI] [PubMed] [Google Scholar]
  7. Dvorak H. F., Simpson B. A., Bast R. C., Jr, Leskowitz S. Cutaneous basophil hypersensitivity. 3. Participation of the basophil in hypersensitivity to antigen-antibody complexes, delayed hypersensitivity and contact allergy. Passive transfer. J Immunol. 1971 Jul;107(1):138–148. [PubMed] [Google Scholar]
  8. Erard D., Charreire J., Auffredou M. T., Galanaud P., Bach J. F. Regulation of contact sensitivity to DNFB in the mouse: effects of adult thymectomy and thymic factor. J Immunol. 1979 Oct;123(4):1573–1576. [PubMed] [Google Scholar]
  9. Hurme M., Karjalainen K., Mäkelä O. Failure to demonstrate public idiotypes on cytolytic cells with specificity for NP-coupled syngeneic cells. Scand J Immunol. 1980;11(3):241–246. doi: 10.1111/j.1365-3083.1980.tb00231.x. [DOI] [PubMed] [Google Scholar]
  10. Imanishi T., Mäkelä O. Inheritance of antibody specificity. I. Anti-(4-hydroxy-3-nitrophenyl)acetyl of the mouse primary response. J Exp Med. 1974 Dec 1;140(6):1498–1510. doi: 10.1084/jem.140.6.1498. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Karjalainen K., Bång B., Mäkelä O. Fine specificity and idiotypes of early antibodies against (4-hydroxy-3-nitrophenyl)acetyl (NP). J Immunol. 1980 Jul;125(1):313–317. [PubMed] [Google Scholar]
  12. Leung K. N., Ada G. L., McKenzie I. F. Specificity, Ly phenotype, and H-2 compatibility requirements of effector cells in delayed-type hypersensitivity responses to murine influenza virus infection. J Exp Med. 1980 Apr 1;151(4):815–826. doi: 10.1084/jem.151.4.815. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Miller J. F., Vadas M. A., Whitelaw A., Gamble J. Role of major histocompatibility complex gene products in delayed-type hypersensitivity. Proc Natl Acad Sci U S A. 1976 Jul;73(7):2486–2490. doi: 10.1073/pnas.73.7.2486. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Rehn T. G., Inman J. K., Shearer G. M. Cell-mediated lympholysis to H-2-matched target cells modified with a series of nitrophenyl compounds. J Exp Med. 1976 Oct 1;144(4):1134–1140. doi: 10.1084/jem.144.4.1134. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Stashenko P., Klinman N. R. Analysis of the primary anti-(4-hydroxy-3-nitrophenyl) acetyl (NP) responsive B cells in BALB/C and B10.D2 mice. J Immunol. 1980 Aug;125(2):531–537. [PubMed] [Google Scholar]
  16. Sunday M. E., Weinberger J. Z., Benacerraf B., Dorf M. E. Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. J Immunol. 1980 Oct;125(4):1601–1605. [PubMed] [Google Scholar]
  17. Tagart V. The secondary cytotoxic response to trinitrophenyl (TNP) modified syngeneic lymphocytes: effectors generated in vitro differ from those generated in vivo. Scand J Immunol. 1978;8(2):91–97. doi: 10.1111/j.1365-3083.1978.tb00500.x. [DOI] [PubMed] [Google Scholar]
  18. Weinberger J. Z., Germain R. N., Benacerraf B., Dorf M. E. Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. V. Role of idiotypes in the suppressor pathway. J Exp Med. 1980 Jul 1;152(1):161–169. doi: 10.1084/jem.152.1.161. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Weinberger J. Z., Germain R. N., Ju S. T., Greene M. I., Benacerraf B., Dorf M. E. Hapten-specific T-cell responses to 4-hydroxy-3-nitrophenyl acetyl. II. Demonstration of idiotypic determinants on suppressor T cells. J Exp Med. 1979 Oct 1;150(4):761–776. doi: 10.1084/jem.150.4.761. [DOI] [PMC free article] [PubMed] [Google Scholar]
  20. Weinberger J. Z., Greene M. I., Benacerraf B., Dorf M. E. Hapten-specific T-cell responses to 4-hydroxy-3-nitrophenyl acetyl. I. Genetic control of delayed-type hypersensitivity by VH and I-A-region genes. J Exp Med. 1979 Jun 1;149(6):1336–1348. doi: 10.1084/jem.149.6.1336. [DOI] [PMC free article] [PubMed] [Google Scholar]
  21. Weiner H. L., Greene M. I., Fields B. N. Delayed hypersensitivity in mice infected with reovirus. I. Identification of host and viral gene products responsible for the immune response. J Immunol. 1980 Jul;125(1):278–282. [PubMed] [Google Scholar]
  22. Zinkernagel R. M. H-2 restriction of virus-specific T-cell-mediated effector functions in vivo. II. Adoptive transfer of delayed-type hypersensitivity to murine lymphocytic choriomeningits virus is restriced by the K and D region of H-2. J Exp Med. 1976 Sep 1;144(3):776–787. doi: 10.1084/jem.144.3.776. [DOI] [PMC free article] [PubMed] [Google Scholar]

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