PMID- 11285114
OWN - NLM
STAT- MEDLINE
DCOM- 20010426
LR  - 20191210
IS  - 0300-9475 (Print)
IS  - 0300-9475 (Linking)
VI  - 53
IP  - 4
DP  - 2001 Apr
TI  - Validity of the two-signal model for activation of CD28-deficient T lymphocytes: 
      quantitative characterization of an alternative costimulatory function of 
      dendritic cells.
PG  - 346-56
AB  - The observation that primary T-dependent immune responses are generated in mice 
      lacking CD28, the only receptor definitively shown to costimulate naive T cells, 
      has led to ambiguity as to whether costimulation is absolutely required for 
      initiation of T-cell responses. In this report, in vitro analysis of the 
      relationship between cell density and proliferation demonstrates that activation 
      of CD28-/- T cells to immobilized T-cell receptor (TCR)-alpha monoclonal 
      antibodies (MoAb) depends on costimulatory signals provided by other cells in 
      culture and occurs only at cell densities sufficient to permit these 
      intercellular interactions. These signals are necessary even under TCR triggering 
      conditions that obviate the CD28 requirement. Dendritic cells (DCs) provide the 
      necessary costimulation in vitro and prime T cells in vivo in CD28-/- mice. 
      Single-cell and limiting dilution analyses indicate that individual T cells from 
      normal and CD28-/- mice produce equivalent interleukin (IL)-2 in response to DCs. 
      However, half as many T cells produce IL-2 when only the CD28-independent pathway 
      is used. Nonetheless, CD28-/- T cells produce sufficient IL-2 to support clonal 
      expansion comparable to that of CD28+/+ T cells, which may account for the 
      equally robust in vivo responses initiated by DCs in normal and CD28-deficient 
      animals.
FAU - Cassell, D J
AU  - Cassell DJ
AD  - The Cancer Research Laboratory, University of California at Berkeley, Berkeley, 
      CA 94720, USA. djtcassell@aol.com
LA  - eng
GR  - CA 09041/CA/NCI NIH HHS/United States
GR  - CA 40041/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Validation Study
PL  - England
TA  - Scand J Immunol
JT  - Scandinavian journal of immunology
JID - 0323767
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antigens, CD)
RN  - 0 (B7-1 Antigen)
RN  - 0 (B7-2 Antigen)
RN  - 0 (CD28 Antigens)
RN  - 0 (Cd86 protein, mouse)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Receptors, Antigen, T-Cell, alpha-beta)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/pharmacology
MH  - Antigens, CD/metabolism
MH  - B7-1 Antigen/metabolism
MH  - B7-2 Antigen
MH  - CD28 Antigens/genetics/*metabolism
MH  - Cell Communication
MH  - Dendritic Cells/*immunology
MH  - In Vitro Techniques
MH  - Lymphocyte Activation
MH  - Membrane Glycoproteins/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - *Models, Biological
MH  - Receptors, Antigen, T-Cell, alpha-beta/antagonists & inhibitors/metabolism
MH  - Signal Transduction
MH  - T-Lymphocytes/*immunology
EDAT- 2001/04/04 10:00
MHDA- 2001/05/01 10:01
CRDT- 2001/04/04 10:00
PHST- 2001/04/04 10:00 [pubmed]
PHST- 2001/05/01 10:01 [medline]
PHST- 2001/04/04 10:00 [entrez]
AID - sji909 [pii]
AID - 10.1046/j.1365-3083.2001.00909.x [doi]
PST - ppublish
SO  - Scand J Immunol. 2001 Apr;53(4):346-56. doi: 10.1046/j.1365-3083.2001.00909.x.