During Viral Infection of the Respiratory Tract, CD27, 4-1BB, and OX40 Collectively Determine Formation of CD8+ Memory T Cells and Their Capacity for Secondary Expansion. Export

@article{citeulike:296484, abstract = {Independent studies have shown that CD27, 4-1BB, and OX40 can all promote survival of activated CD8(+) T cells. We have therefore compared their impact on CD8(+) memory T cell formation and responsiveness within one, physiologically relevant model system. Recombinant mice, selectively lacking input of one or two receptors, were challenged intranasally with influenza virus, and the immunodominant virus-specific CD8(+) T cell response was quantified at priming and effector sites. Upon primary infection, CD27 and (to a lesser extent) 4-1BB made nonredundant contributions to accumulation of CD8(+) virus-specific T cells in draining lymph nodes and lung, while OX40 had no effect. Interestingly though, in the memory response, accumulation of virus-specific CD8(+) T cells in spleen and lung critically depended on all three receptor systems. This was explained by two observations: 1) CD27, 4-1BB, and OX40 were collectively responsible for generation of the same memory CD8(+) T cell pool; 2) CD27, 4-1BB, and OX40 collectively determined the extent of secondary expansion, as shown by adoptive transfers with standardized numbers of memory cells. Surprisingly, wild-type CD8(+) memory T cells expanded normally in primed OX40 ligand- or 4-1BB ligand-deficient mice. However, when wild-type memory cells were generated in OX40 ligand- or 4-1BB ligand-deficient mice, their secondary expansion was impaired. This provides the novel concept that stimulation of CD8(+) T cells by OX40 and 4-1BB ligand during priming imprints into them the capacity for secondary expansion. Our data argue that ligand on dendritic cells and/or B cells may be critical for this.}, address = {Division of Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.}, author = {Hendriks, J. and Xiao, Y. and Rossen, J. W. and van der Sluijs, K. F. and Sugamura, K. and Ishii, N. and Borst, J.}, citeulike-article-id = {296484}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/16034107}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=16034107}, day = {1}, issn = {0022-1767}, journal = {J Immunol}, keywords = {4-1bb, cd27, cd4, cd8, determine, expansion, formation, help, memory, ox40, secondary, tcell}, month = {August}, number = {3}, pages = {1665--1676}, posted-at = {2008-10-21 21:46:33}, priority = {2}, title = {During Viral Infection of the Respiratory Tract, CD27, 4-1BB, and OX40 Collectively Determine Formation of CD8+ Memory T Cells and Their Capacity for Secondary Expansion.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/16034107}, volume = {175}, year = {2005} }

TY - JOUR ID - citeulike:296484 L3 - citeulike-article-id:296484 N2 - Independent studies have shown that CD27, 4-1BB, and OX40 can all promote survival of activated CD8(+) T cells. We have therefore compared their impact on CD8(+) memory T cell formation and responsiveness within one, physiologically relevant model system. Recombinant mice, selectively lacking input of one or two receptors, were challenged intranasally with influenza virus, and the immunodominant virus-specific CD8(+) T cell response was quantified at priming and effector sites. Upon primary infection, CD27 and (to a lesser extent) 4-1BB made nonredundant contributions to accumulation of CD8(+) virus-specific T cells in draining lymph nodes and lung, while OX40 had no effect. Interestingly though, in the memory response, accumulation of virus-specific CD8(+) T cells in spleen and lung critically depended on all three receptor systems. This was explained by two observations: 1) CD27, 4-1BB, and OX40 were collectively responsible for generation of the same memory CD8(+) T cell pool; 2) CD27, 4-1BB, and OX40 collectively determined the extent of secondary expansion, as shown by adoptive transfers with standardized numbers of memory cells. Surprisingly, wild-type CD8(+) memory T cells expanded normally in primed OX40 ligand- or 4-1BB ligand-deficient mice. However, when wild-type memory cells were generated in OX40 ligand- or 4-1BB ligand-deficient mice, their secondary expansion was impaired. This provides the novel concept that stimulation of CD8(+) T cells by OX40 and 4-1BB ligand during priming imprints into them the capacity for secondary expansion. Our data argue that ligand on dendritic cells and/or B cells may be critical for this. IS - 3 JF - J Immunol SN - 0022-1767 AD - Division of Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands. EP - 1676 TI - During Viral Infection of the Respiratory Tract, CD27, 4-1BB, and OX40 Collectively Determine Formation of CD8+ Memory T Cells and Their Capacity for Secondary Expansion. VL - 175 SP - 1665 KW - 4-1bb KW - cd27 KW - cd4 KW - cd8 KW - determine KW - expansion KW - formation KW - help KW - memory KW - ox40 KW - secondary KW - tcell AU - Hendriks, J AU - Xiao, Y AU - Rossen, JW AU - van der Sluijs, KF AU - Sugamura, K AU - Ishii, N AU - Borst, J PY - 2005/08/01/ UR - http://view.ncbi.nlm.nih.gov/pubmed/16034107 ER -