T Memory Cells in a Model of T Cell Memory

Author(s):  
Angela R. McLean
2008 ◽  
Vol 118 (1) ◽  
pp. 294-305 ◽  
Author(s):  
Carolina Berger ◽  
Michael C. Jensen ◽  
Peter M. Lansdorp ◽  
Mike Gough ◽  
Carole Elliott ◽  
...  

2004 ◽  
Vol 65 (9-10) ◽  
pp. S66
Author(s):  
Kathy Spichty ◽  
Kevin McDade ◽  
Husain Shahid ◽  
Carol Bentlejewski ◽  
Alin Girnita ◽  
...  

Blood ◽  
2010 ◽  
Vol 115 (9) ◽  
pp. 1678-1689 ◽  
Author(s):  
Jeffrey D. Ahlers ◽  
Igor M. Belyakov

Abstract For acute self-limiting infections a vaccine is successful if it elicits memory at least as good as the natural experience; however, for persistent and chronic infections such as HIV, hepatitis C virus (HCV), human papillomavirus (HPV), and human herpes viruses, this paradigm is not applicable. At best, during persistent virus infection the person must be able to maintain the integrity of the immune system in equilibrium with controlling replicating virus. New vaccine strategies are required that elicit both potent high-avidity CD8+ T-cell effector/memory and central memory responses that can clear the nidus of initial virus-infected cells at mucosal surfaces to prevent mucosal transmission or significantly curtail development of disease. The objective of an HIV-1 T-cell vaccine is to generate functional CD8+ effector memory cells at mucosal portals of virus entry to prevent viral transmission. In addition, long-lived CD8+ and CD4+ central memory cells circulating through secondary lymphoid organs and resident in bone marrow, respectively, are needed to provide a concerted second wave of defense that can contain virus at mucosal surfaces and prevent systemic dissemination. Further understanding of factors which can influence long-lived effector and central memory cell differentiation will significantly contribute to development of effective T-cell vaccines. In this review we will focus on discussing mechanisms involved in T-cell memory and provide promising new approaches toward expanding current vaccine strategies to enhance antiviral memory.


1991 ◽  
Vol 174 (5) ◽  
pp. 969-974 ◽  
Author(s):  
D Gray ◽  
P Matzinger

Immunological memory has generally been ascribed to the development of long-lived memory cells that can persist for years in the absence of renewed antigenic encounter. In the experiments reported here, we have adoptively transferred memory T cells in the presence and absence of priming antigen and assessed their functional survival. The results indicate that, in contrast to the traditional view, the maintenance of T cell memory requires the presence of antigen, suggesting that memory, like tolerance, is an antigen-dependent process rather than an antigen-independent state.


2015 ◽  
Vol 22 (5) ◽  
pp. 561-569 ◽  
Author(s):  
Lia de Rond ◽  
Rose-Minke Schure ◽  
Kemal Öztürk ◽  
Guy Berbers ◽  
Elisabeth Sanders ◽  
...  

ABSTRACTWhooping cough remains a problem despite vaccination, and worldwide resurgence of pertussis is evident. Since cellular immunity plays a role in long-term protection against pertussis, we studied pertussis-specific T-cell responses. Around the time of the preschool acellular pertussis (aP) booster dose at 4 years of age, T-cell memory responses were compared in children who were primed during infancy with either a whole-cell pertussis (wP) or an aP vaccine. Peripheral blood mononuclear cells (PBMCs) were isolated and stimulated with pertussis vaccine antigens for 5 days. T cells were characterized by flow-based analysis of carboxyfluorescein succinimidyl ester (CFSE) dilution and CD4, CD3, CD45RA, CCR7, gamma interferon (IFN-γ), and tumor necrosis factor alpha (TNF-α) expression. Before the aP preschool booster vaccination, both the proliferated pertussis toxin (PT)-specific CD4+and CD8+T-cell fractions (CFSEdim) were higher in aP- than in wP-primed children. Post-booster vaccination, more pertussis-specific CD4+effector memory cells (CD45RA−CCR7−) were induced in aP-primed children than in those primed with wP. The booster vaccination did not appear to significantly affect the T-cell memory subsets and functionality in aP-primed or wP-primed children. Although the percentages of Th1 cytokine-producing cells were alike in aP- and wP-primed children pre-booster vaccination, aP-primed children produced more Th1 cytokines due to higher numbers of proliferated pertussis-specific effector memory cells. At present, infant vaccinations with four aP vaccines in the first year of life result in pertussis-specific CD4+and CD8+effector memory T-cell responses that persist in children until 4 years of age and are higher than those in wP-primed children. The booster at 4 years of age is therefore questionable; this may be postponed to 6 years of age.


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