PMID- 9840700
OWN - NLM
STAT- MEDLINE
DCOM- 19990308
LR  - 20190516
IS  - 0918-2918 (Print)
IS  - 0918-2918 (Linking)
VI  - 37
IP  - 10
DP  - 1998 Oct
TI  - Modification of human T-cell responses by altered peptide ligands: a new approach 
      to antigen-specific modification.
PG  - 804-17
AB  - Human CD4+ T-cells recognize antigenic peptides in the context of human leukocyte 
      antigen (HLA) class II molecules and produce various lymphokines to proliferate 
      and activate other cells. It was once considered that the T-cell response is an 
      all or nothing type event, but recent studies have clearly indicated that T-cells 
      show many different types of activation in recognition of altered ligands for 
      T-cell receptors (TCR). In this review, we summarize our recent findings on the 
      human CD4+ T-cell response to altered peptide ligands (APL); peptides carrying 
      single residue substitutions in antigenic peptides. We observed the following: 1) 
      TCR antagonism for T-cell clones reactive to non-self or autoantigenic peptides, 
      2) partial activation (agonism) without cell proliferation, including production 
      of lymphokines and increases in cell size, and in expression levels of several 
      cell surface proteins or survival time in the absence of antigenic stimulus, 3) 
      augmentation in cell proliferation and production of interferon-gamma (IFN-gamma) 
      and granulocyte monocyte colony stimulating factor (GM-CSF), 4) augmentation of 
      interleukin (IL)-12 production by antigen presenting cell (APC) and the 
      subsequent augmented production of IFN-gamma by T-cells. This information 
      provides basic knowledge regarding the characteristics of T-cell recognition of 
      antigens and the subsequent activation, and a novel method for modification of 
      human T-cell responses by altered peptide ligands (APLs), as a possible candidate 
      for antigen-specific immunopotentiating or immunosuppressive therapy against 
      autoimmune diseases, allergies, infectious diseases and malignant tumors.
FAU - Nishimura, Y
AU  - Nishimura Y
AD  - Department of Neuroscience and Immunology, Kumamoto University Graduate School of 
      Medical Sciences.
FAU - Chen, Y Z
AU  - Chen YZ
FAU - Kanai, T
AU  - Kanai T
FAU - Yokomizo, H
AU  - Yokomizo H
FAU - Matsuoka, T
AU  - Matsuoka T
FAU - Matsushita, S
AU  - Matsushita S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Japan
TA  - Intern Med
JT  - Internal medicine (Tokyo, Japan)
JID - 9204241
RN  - 0 (Antigens)
RN  - 0 (Antigens, Bacterial)
RN  - 0 (Autoantigens)
RN  - 0 (BCL2L1 protein, human)
RN  - 0 (Bcl2l1 protein, mouse)
RN  - 0 (HLA-D Antigens)
RN  - 0 (Ligands)
RN  - 0 (Lymphokines)
RN  - 0 (Peptide Fragments)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Receptors, Antigen, T-Cell)
RN  - 0 (Receptors, Cholinergic)
RN  - 0 (bcl-X Protein)
RN  - EC 3.6.5.2 (HRAS protein, human)
RN  - EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
SB  - IM
MH  - Adoptive Transfer
MH  - Amino Acid Sequence
MH  - Amino Acid Substitution
MH  - Animals
MH  - Antigen Presentation
MH  - Antigens/immunology
MH  - Antigens, Bacterial/immunology
MH  - Apoptosis
MH  - Autoantigens/immunology
MH  - Autoimmune Diseases/immunology
MH  - CD4-Positive T-Lymphocytes/*immunology/metabolism
MH  - Clone Cells/immunology
MH  - HLA-D Antigens/immunology
MH  - Humans
MH  - Infant
MH  - Ligands
MH  - *Lymphocyte Activation
MH  - Lymphokines/metabolism
MH  - Mice
MH  - Mites/immunology
MH  - Molecular Sequence Data
MH  - Myasthenia Gravis/immunology
MH  - Mycobacterium bovis/immunology
MH  - Peptide Fragments/chemistry/*immunology
MH  - Proto-Oncogene Proteins c-bcl-2/biosynthesis/genetics
MH  - Proto-Oncogene Proteins p21(ras)/chemistry/immunology
MH  - Receptors, Antigen, T-Cell/chemistry/*immunology
MH  - Receptors, Cholinergic/immunology
MH  - T-Lymphocyte Subsets/immunology
MH  - bcl-X Protein
RF  - 96
EDAT- 1998/12/05 00:00
MHDA- 1998/12/05 00:01
CRDT- 1998/12/05 00:00
PHST- 1998/12/05 00:00 [pubmed]
PHST- 1998/12/05 00:01 [medline]
PHST- 1998/12/05 00:00 [entrez]
AID - 10.2169/internalmedicine.37.804 [doi]
PST - ppublish
SO  - Intern Med. 1998 Oct;37(10):804-17. doi: 10.2169/internalmedicine.37.804.