scholarly journals Efficient Development ofPlasmodiumLiver Stage–Specific Memory CD8+T Cells during the Course of Blood‐Stage Malarial Infection

2007 ◽  
Vol 196 (12) ◽  
pp. 1827-1835 ◽  
Author(s):  
Julius C. R. Hafalla ◽  
Urvashi Rai ◽  
Dabeiba Bernal‐Rubio ◽  
Ana Rodriguez ◽  
Fidel Zavala
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Blood Stage ◽  
Memory Cd8 T Cells ◽  
Malarial Infection ◽  
Specific Memory

Cognate CD4 help is essential for the reactivation and expansion of CD8 memory T cells directed against the hematopoietic cell–specific dominant minor histocompatibility antigen, H60

Blood ◽  
2009 ◽  
Vol 113 (18) ◽  
pp. 4273-4280 ◽  
Author(s):  
Su Jeong Ryu ◽  
Kyung Min Jung ◽  
Hyun Seung Yoo ◽  
Tae Woo Kim ◽  
Sol Kim ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Primary Response ◽  
Hematopoietic Cell ◽  
Secondary Response ◽  
Memory Cd8 T Cells ◽  
Specific Memory ◽  
Cd4 Help ◽  
Different Response

AbstractIn contrast to previous notions of the help-independency of memory CD8 T cells during secondary expansion, here we show that CD4 help is indispensable for the re-expansion of once-helped memory CD8 T cells, using a hematopoietic cell–specific dominant minor histocompatibility (H) antigen, H60, as a model antigen. H60-specific memory CD8 T cells generated during a helped primary response vigorously expanded only when rechallenged under helped conditions. The help requirement for an optimal secondary response was confirmed by a reduction in peak size by CD4 depletion, and was reproduced after skin transplantation. Helpless conditions or noncognate separate help during the secondary response resulted in a significant reduction in the peak size and different response kinetics. Providing CD4 help again during a tertiary challenge restored robust memory expansion; however, the repeated deprivation of help further reduced clonal expansion. Adoptively transferred memory CD8 T cells did not proliferate in CD40L−/− hosts. In the CD40−/− hosts, marginal memory expansion was detected after priming with male H60 cells but was completely abolished by priming with peptide-loaded CD40−/− cells, suggesting the essential role of CD40 and CD40L in memory responses. These results provide insight into the control of minor H antigen-specific CD8 T-cell responses, to maximize the graft-versus-leukemia response.

scholarly journals PD1 is expressed on exhausted T cells as well as virus specific memory CD8+ T cells in the bone marrow of myeloma patients

Oncotarget ◽  
2018 ◽  
Vol 9 (62) ◽  
pp. 32024-32035 ◽  
Author(s):  
Anne-Marit Sponaas ◽  
Rui Yang ◽  
Even Holth Rustad ◽  
Therese Standal ◽  
Aud Solvang Thoresen ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Cd8 T Cells ◽  
Memory Cd8 T Cells ◽  
Specific Memory

scholarly journals The route of priming influences the ability of respiratory virus–specific memory CD8+ T cells to be activated by residual antigen

2010 ◽  
Vol 207 (6) ◽  
pp. 1153-1160 ◽  
Author(s):  
Shiki Takamura ◽  
Alan D. Roberts ◽  
Dawn M. Jelley-Gibbs ◽  
Susan T. Wittmer ◽  
Jacob E. Kohlmeier ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Cd8 T Cells ◽  
Respiratory Virus ◽  
Virus Infections ◽  
Memory Cd8 T Cells ◽  
Virus Clearance ◽  
Specific Memory ◽  
Respiratory Virus Infections ◽  
Lung Airways

After respiratory virus infections, memory CD8+ T cells are maintained in the lung airways by a process of continual recruitment. Previous studies have suggested that this process is controlled, at least in the initial weeks after virus clearance, by residual antigen in the lung-draining mediastinal lymph nodes (MLNs). We used mouse models of influenza and parainfluenza virus infection to show that intranasally (i.n.) primed memory CD8+ T cells possess a unique ability to be reactivated by residual antigen in the MLN compared with intraperitoneally (i.p.) primed CD8+ T cells, resulting in the preferential recruitment of i.n.-primed memory CD8+ T cells to the lung airways. Furthermore, we demonstrate that the inability of i.p.-primed memory CD8+ T cells to access residual antigen can be corrected by a subsequent i.n. virus infection. Thus, two independent factors, initial CD8+ T cell priming in the MLN and prolonged presentation of residual antigen in the MLN, are required to maintain large numbers of antigen-specific memory CD8+ T cells in the lung airways.

scholarly journals Requirement of Mature Dendritic Cells for Efficient Activation of Influenza A-Specific Memory CD8+T Cells

2000 ◽  
Vol 165 (3) ◽  
pp. 1182-1190 ◽  
Author(s):  
Marie Larsson ◽  
Davorka Messmer ◽  
Selin Somersan ◽  
Jean-François Fonteneau ◽  
Sean M. Donahoe ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cd8 T Cells ◽  
Influenza A ◽  
Memory Cd8 T Cells ◽  
Specific Memory

scholarly journals APC‐targeted proinsulin expression inactivates insulin‐specific memory CD8 + T cells in NOD mice

2017 ◽  
Vol 95 (9) ◽  
pp. 765-774 ◽  
Author(s):  
Peta LS Reeves ◽  
Rajeev Rudraraju ◽  
Xiao Liu ◽  
F Susan Wong ◽  
Emma E Hamilton‐Williams ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Nod Mice ◽  
Memory Cd8 T Cells ◽  
Specific Memory

scholarly journals Attrition of Bystander CD8 T Cells during Virus-Induced T-Cell and Interferon Responses

2001 ◽  
Vol 75 (13) ◽  
pp. 5965-5976 ◽  
Author(s):  
James M. McNally ◽  
Christopher C. Zarozinski ◽  
Meei-Yun Lin ◽  
Michael A. Brehm ◽  
Hong D. Chen ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Lymphocytic Choriomeningitis ◽  
T Cell Response ◽  
Poly I:C ◽  
Memory Cd8 T Cells ◽  
Specific Memory ◽  
Specific Expansion ◽  
Β Receptor

ABSTRACT Experiments designed to distinguish virus-specific from non-virus-specific T cells showed that bystander T cells underwent apoptosis and substantial attrition in the wake of a strong T-cell response. Memory CD8 T cells (CD8+ CD44hi) were most affected. During acute viral infection, transgenic T cells that were clearly defined as non-virus specific decreased in number and showed an increase in apoptosis. Also, use of lymphocytic choriomeningitis virus (LCMV) carrier mice, which lack LCMV-specific T cells, showed a significant decline in non-virus-specific memory CD8 T cells that correlated to an increase in apoptosis in response to the proliferation of adoptively transferred virus-specific T cells. Attrition of T cells early during infection correlated with the alpha/beta interferon (IFN-α/β) peak, and the IFN inducer poly(I:C) caused apoptosis and attrition of CD8+CD44hi T cells in normal mice but not in IFN-α/β receptor-deficient mice. Apoptotic attrition of bystander T cells may make room for the antigen-specific expansion of T cells during infection and may, in part, account for the loss of T-cell memory that occurs when the host undergoes subsequent infections.

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