PMID- 21453718
OWN - NLM
STAT- MEDLINE
DCOM- 20110906
LR  - 20171116
IS  - 1872-6216 (Electronic)
IS  - 0047-6374 (Linking)
VI  - 132
IP  - 4
DP  - 2011 Apr
TI  - Impaired in vivo CD4+ T cell expansion and differentiation in aged mice is not 
      solely due to T cell defects: decreased stimulation by aged dendritic cells.
PG  - 187-94
LID - 10.1016/j.mad.2011.03.005 [doi]
AB  - CD4+ T cells regulate humoral and cell-mediated immune responses, which are 
      progressively impaired in aging, resulting in susceptibility to infections and 
      cancer. Dendritic cells (DCs) are major activators of T cells, providing signals 
      that drive their expansion and differentiation. In this study, we asked if 
      decreased CD4+ T cell responses were influenced by the age of DCs rather than 
      being exclusively due to T cell defects. Old T cells transferred to young 
      recipients expanded and differentiated similarly to young T cells. However, aged 
      recipients were poor stimulators of both old and young T cells, which failed to 
      acquire CD44 expression and produce interferon gamma (IFN-gamma). DCs in aged hosts 
      expressed fewer MHC-peptide complexes. The CD86 expression in the DCs of both 
      hosts was similar; however, CD40 levels were reduced in old DCs. Finally, old DCs 
      failed to produce inflammatory cytokines in response to LPS. Our results indicate 
      that the impairment of aged CD4+ T cell function is intimately related to 
      multiple alterations in aged DCs, rather than being caused solely by intrinsic T 
      cell defects, suggesting that the function of aged T cells may be partially 
      rescued in vivo when appropriate stimulation is applied. These findings are 
      relevant to vaccination design for elderly populations.
CI  - Copyright (c) 2011. Published by Elsevier Ireland Ltd.
FAU - Pereira, Luciana F
AU  - Pereira LF
AD  - Departamento de Biologia Celular e Molecular (FABIO) and Instituto de Pesquisas 
      Biomedicas, PUCRS, Av. Ipiranga, Porto Alegre, RS, Brazil.
FAU - de Souza, Ana Paula Duarte
AU  - de Souza AP
FAU - Borges, Thiago J
AU  - Borges TJ
FAU - Bonorino, Cristina
AU  - Bonorino C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110329
PL  - Ireland
TA  - Mech Ageing Dev
JT  - Mechanisms of ageing and development
JID - 0347227
RN  - 0 (CD40 Antigens)
RN  - 0 (Cytokines)
RN  - 0 (Hyaluronan Receptors)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Peptides)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Age Factors
MH  - Aging
MH  - Animals
MH  - Antigen Presentation
MH  - CD4-Positive T-Lymphocytes/*cytology
MH  - CD40 Antigens/biosynthesis
MH  - Cell Differentiation
MH  - Cytokines/metabolism
MH  - Dendritic Cells/*cytology
MH  - Hyaluronan Receptors/biosynthesis
MH  - Interferon-gamma/metabolism
MH  - Lipopolysaccharides/metabolism
MH  - Major Histocompatibility Complex
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Peptides/chemistry
EDAT- 2011/04/02 06:00
MHDA- 2011/09/07 06:00
CRDT- 2011/04/02 06:00
PHST- 2010/07/23 00:00 [received]
PHST- 2011/03/09 00:00 [revised]
PHST- 2011/03/18 00:00 [accepted]
PHST- 2011/04/02 06:00 [entrez]
PHST- 2011/04/02 06:00 [pubmed]
PHST- 2011/09/07 06:00 [medline]
AID - S0047-6374(11)00044-3 [pii]
AID - 10.1016/j.mad.2011.03.005 [doi]
PST - ppublish
SO  - Mech Ageing Dev. 2011 Apr;132(4):187-94. doi: 10.1016/j.mad.2011.03.005. Epub 
      2011 Mar 29.