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A human CD4- T cell leukemia subclone with contact-dependent helper function.

M J Yellin1, J J Lee, L Chess

  • 1Department of Medicine, Columbia University, New York, NY 10032.

Journal of Immunology (Baltimore, Md. : 1950)
|November 15, 1991
PubMed
Summary
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A specific T cell clone (D1.1) activates resting B cells through direct contact, promoting their differentiation into antibody-secreting cells. This contact-dependent B cell activation is mediated by surface molecules, not secreted factors.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Helper T lymphocytes are crucial for B cell differentiation into antibody-secreting cells.
  • The specific surface molecules on T cells responsible for this helper function remain largely unidentified.

Purpose of the Study:

  • To investigate the role of T cell surface structures in mediating contact-dependent B cell activation.
  • To characterize the B cell activating properties of a unique CD4- T cell subclone (D1.1).

Main Methods:

  • Coculture of resting B cells with the Jurkat D1.1 T cell subclone.
  • Analysis of B cell surface marker expression (CD23) and proliferation.
  • Assessment of B cell differentiation into IgG-secreting cells.
  • Testing the activity of fixed cells, supernatants, and the effect of anti-IL-4 antibodies.

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Main Results:

  • Jurkat D1.1 induced B cell expression of CD23, a marker of B cell activation.
  • D1.1 promoted B cell proliferation and differentiation into IgG-secreting cells.
  • The B cell activation was contact-dependent, mediated by surface structures on D1.1, and not inhibited by anti-IL-4 antibodies.

Conclusions:

  • Surface molecules on activated T cells mediate contact-dependent B cell activation.
  • The Jurkat D1.1 subclone provides a model for studying T cell-B cell interactions.
  • This interaction is independent of antigen specificity and MHC restriction.