Responsiveness of T lymphocytes from systemic lupus erythematosus to signals provided through CD26 antigen

Clin Immunol Immunopathol. 1994 Aug;72(2):227-32. doi: 10.1006/clin.1994.1135.


To investigate whether the T cell defective capacity to proliferate observed in systemic lupus erythematosus (SLE) T cells is a possible consequence of an intrinsic T cell disorder, the integrity of the accessory activation pathway mediated through CD26 antigen in SLE T cells was studied. Hyporesponsiveness of peripheral blood mononuclear cells (PBMC) from SLE to PHA and CD26 Mab was observed and no differences were found when the responsiveness of highly purified T cells to IL-2, IL-2 plus CD26 Mab, phorbol 12-myristate 13-acetate (PMA), or when PMA plus CD26 Mab was analyzed. Findings suggest that signals induced by triggering CD26 are not intrinsically altered in SLE T cells. However, some alteration of the regulatory involvement of monocytes or B cell over T cell function may be involved.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antibodies, Monoclonal / pharmacology
  • Antigens, Differentiation, T-Lymphocyte / immunology
  • Antigens, Differentiation, T-Lymphocyte / physiology*
  • Dipeptidyl Peptidase 4
  • Humans
  • Interleukin-2 / pharmacology
  • Lupus Erythematosus, Systemic / blood
  • Lupus Erythematosus, Systemic / immunology
  • Lupus Erythematosus, Systemic / physiopathology*
  • Lymphocyte Activation / drug effects
  • Lymphocyte Activation / immunology
  • Lymphocyte Activation / physiology*
  • Middle Aged
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*
  • T-Lymphocytes / immunology
  • T-Lymphocytes / physiology*
  • Tetradecanoylphorbol Acetate / pharmacology


  • Antibodies, Monoclonal
  • Antigens, Differentiation, T-Lymphocyte
  • Interleukin-2
  • Dipeptidyl Peptidase 4
  • Tetradecanoylphorbol Acetate