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Lukacs NW, Boros DL. Splenic and granuloma T-lymphocyte responses to fractionated soluble egg antigens of Schistosoma mansoni-infected mice. Infect Immun. 1991;59(3):941-8doi: 10.1128/iai.59.3.941-948.1991.
Lukacs, N. W., & Boros, D. L. (1991). Splenic and granuloma T-lymphocyte responses to fractionated soluble egg antigens of Schistosoma mansoni-infected mice. Infection and immunity, 59(3), 941-8. https://doi.org/10.1128/iai.59.3.941-948.1991
Lukacs, N W, and Boros, D L. "Splenic and granuloma T-lymphocyte responses to fractionated soluble egg antigens of Schistosoma mansoni-infected mice." Infection and immunity vol. 59,3 (1991): 941-8. doi: https://doi.org/10.1128/iai.59.3.941-948.1991
Lukacs NW, Boros DL. Splenic and granuloma T-lymphocyte responses to fractionated soluble egg antigens of Schistosoma mansoni-infected mice. Infect Immun. 1991 Mar;59(3):941-8. doi: 10.1128/iai.59.3.941-948.1991. PMID: 1900066; PMCID: PMC258350.
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Atypon Free PMC Article

Infect Immun. 1991 Mar;59(3):941-8. doi: 10.1128/iai.59.3.941-948.1991.

Splenic and granuloma T-lymphocyte responses to fractionated soluble egg antigens of Schistosoma mansoni-infected mice.

Infection and immunity

N W Lukacs, D L Boros

Affiliations

  1. Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, Michigan 48201.

PMID: 1900066 PMCID: PMC258350 DOI: 10.1128/iai.59.3.941-948.1991
Free PMC Article

Abstract

Soluble egg antigens (SEA) secreted by the eggs of Schistosoma mansoni worms induce a T-cell-mediated granulomatous response that is principally responsible for the pathology of the disease. In the present study sodium dodecyl sulfate-polyacrylamide gel electrophoresis-separated SEA proteins were divided into nine fractions (less than 21, 25 to 30, 32 to 38, 40 to 46, 50 to 56, 60 to 66, 70 to 90, 93 to 125, and greater than 200 kDa), electroeluted, and utilized in in vitro lymphoproliferation assays. T-cell-enriched spleen cells from acutely infected mice responded to all nine fractions, while those from chronically infected mice responded to only the 50- to 56- and the 60- to 66-kDa fractions. Depletion of the CD4+ T-cell subset among acute and chronic-infection spleen cells abrogated the response. Depletion of the CD8+ T-cell population resulted in increased proliferation in response to fractions by acute-infection T cells and facilitated responsiveness to hitherto-inactive SEA fractions in chronic-infection T cells. Acute-infection CD4+ granuloma T cells responded to the 40- to 46-, 50- to 56-, 70- to 90-, 93- to 125-, and greater than 200-kDa fractions, while the chronic-infection granuloma T cells responded only to the greater than 200-kDa fraction of SEA. Selective depletion of the CD4+ T-cell subset when acute-infection granuloma lymphocytes were tested abrogated proliferation, whereas subset depletions when chronic-infection granuloma cells were tested indicated that both CD4+ and CD8+ T cells respond to the greater than 200-kDa fraction. The present study reveals differences between acute- and chronic-infection splenic and granuloma T cells in the pattern of T-cell blastogenic responses to fractionated SEA.

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References

  1. Proc Soc Exp Biol Med. 1956 Aug-Sep;92(4):780-2 - PubMed
  2. Nature. 1970 Aug 15;227(5259):680-5 - PubMed
  3. J Immunol. 1988 Sep 1;141(5):1714-9 - PubMed
  4. Int Arch Allergy Appl Immunol. 1986;81(2):129-35 - PubMed
  5. Exp Parasitol. 1987 Oct;64(2):228-36 - PubMed
  6. J Immunol. 1989 Feb 1;142(3):985-91 - PubMed
  7. J Immunol. 1986 Jun 1;136(11):4275-82 - PubMed
  8. J Immunol. 1986 Feb 1;136(3):1093-9 - PubMed
  9. J Immunol. 1985 Aug;135(2):1421-9 - PubMed
  10. Immunol Suppl. 1989;2:9-14; discussion 15 - PubMed
  11. J Immunol. 1989 May 1;142(9):3239-46 - PubMed
  12. Science. 1989 Jul 14;245(4914):147-53 - PubMed
  13. Clin Microbiol Rev. 1989 Jul;2(3):250-69 - PubMed
  14. J Immunol. 1989 Mar 15;142(6):2061-6 - PubMed
  15. Infect Immun. 1989 Aug;57(8):2475-80 - PubMed
  16. J Immunol. 1985 Mar;134(3):1961-7 - PubMed
  17. Am J Pathol. 1967 Nov;51(5):735-56 - PubMed
  18. Parasitol Today. 1986 Nov;2(11):296-302 - PubMed
  19. J Immunol. 1990 Jul 15;145(2):724-31 - PubMed
  20. J Immunol. 1984 Apr;132(4):2084-8 - PubMed
  21. J Immunol. 1982 Apr;128(4):1864-9 - PubMed
  22. J Exp Med. 1980 Jun 1;151(6):1398-412 - PubMed
  23. J Exp Med. 1983 Jan 1;157(1):219-30 - PubMed
  24. J Exp Med. 1984 May 1;159(5):1371-87 - PubMed
  25. Parasite Immunol. 1983 Sep;5(5):499-511 - PubMed
  26. Immunol Rev. 1982;61:189-213 - PubMed
  27. Trans R Soc Trop Med Hyg. 1981;75(1):54-71 - PubMed
  28. Proc Natl Acad Sci U S A. 1981 Feb;78(2):1152-6 - PubMed
  29. J Immunol. 1981 Jul;127(1):363-7 - PubMed
  30. J Immunol. 1982 Jan;128(1):37-42 - PubMed
  31. J Immunol. 1982 Jan;128(1):30-6 - PubMed
  32. Cell Immunol. 1979 Aug;46(1):192-200 - PubMed
  33. J Immunol. 1979 Jan;122(1):39-43 - PubMed
  34. J Immunol. 1979 Sep;123(3):1409-14 - PubMed
  35. J Immunol. 1979 Jun;122(6):2204-9 - PubMed
  36. J Immunol. 1977 Oct;119(4):1275-8 - PubMed
  37. J Immunol. 1977 Jan;118(1):373-6 - PubMed
  38. J Immunol. 1976 Nov;117(5 Pt 1):1553-60 - PubMed
  39. Eur J Immunol. 1973 Oct;3(10):645-9 - PubMed
  40. J Infect Dis. 1974 Nov;130(5):515-22 - PubMed
  41. J Immunol. 1975 May;114(5):1437-41 - PubMed
  42. J Immunol. 1975 Jul;115(1):150-6 - PubMed
  43. J Exp Med. 1970 Sep 1;132(3):488-507 - PubMed
  44. J Immunol. 1988 May 1;140(9):3273-9 - PubMed

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