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In vivo antagonism of a T cell response by an endogenously expressed ligand. Proc Natl Acad Sci U S A 1998 Nov 24;95(24):14332-6

Date

11/25/1998

Pubmed ID

9826700

Pubmed Central ID

PMC24373

DOI

10.1073/pnas.95.24.14332

Scopus ID

2-s2.0-0032564340   35 Citations

Abstract

3.L2 T cell receptor transgenic T cells are activated by the 64-76 peptide of the mouse hemoglobin d beta chain [Hb(64-76)], and their response is antagonized by the position 72 alanine substitution of this peptide (A72). To test the effect of this altered peptide ligand (APL) on 3.L2 T cell function in vivo, a transgene expressing A72 in major histocompatibility complex II positive cells (A72tg) has been introduced into mice. We demonstrate that 3.L2 T cells, when transferred to A72tg+ mice show a dramatically reduced proliferative response to Hb(64-76). Identical decreased responses were observed using T cells that developed in either A72tg+ or A72tg- hosts. This affect was not attributable to diminished precursor frequency, anergy, or competition for binding to I-Ek molecules. These results unequivocally demonstrate in vivo antagonism by an endogenous APL and characterize a class of self-peptides that, although inefficient in causing deletion in the thymus, effectively modulate T cell responses in the periphery.

Author List

Basu D, Williams CB, Allen PM

Author

Calvin B. Williams MD, PhD Chief, Professor in the Pediatrics department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Alleles
Amino Acid Sequence
Animals
Cells, Cultured
Crosses, Genetic
Flow Cytometry
Hemoglobins, Abnormal
Histocompatibility Antigens Class II
Lymphocyte Activation
Mice
Mice, Transgenic
Peptide Fragments
Receptors, Antigen, T-Cell
T-Lymphocytes