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Journal articles on the topic 'Memory Affinity'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Fishman, Michael A., and Alan S. Perelson. "Lymphocyte memory and affinity selection." Journal of Theoretical Biology 173, no. 3 (April 1995): 241–62. http://dx.doi.org/10.1016/s0022-5193(95)80003-4.

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2

Nikolopoulos, D. S., E. Artiaga, E. Ayguadé, and J. Labarta. "Exploiting memory affinity in OpenMP through schedule reuse." ACM SIGARCH Computer Architecture News 29, no. 5 (December 2001): 49–55. http://dx.doi.org/10.1145/563647.563657.

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3

Ji, Minwen. "Affinity-based management of main memory database clusters." ACM Transactions on Internet Technology 2, no. 4 (November 2002): 307–39. http://dx.doi.org/10.1145/604596.604599.

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4

Shimoda, Michiko, Toru Nakamura, Yoshimasa Takahashi, Hideki Asanuma, Shin-ichi Tamura, Takeshi Kurata, Tsuguo Mizuochi, Norihiro Azuma, Choemon Kanno, and Toshitada Takemori. "Isotype-specific Selection of High Affinity Memory B Cells in Nasal-associated Lymphoid Tissue." Journal of Experimental Medicine 194, no. 11 (December 3, 2001): 1597–608. http://dx.doi.org/10.1084/jem.194.11.1597.

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Mucosal immunoglobulin (Ig)A dominance has been proposed to be associated with preferential class switch recombination (CSR) to the IgA heavy chain constant region, Cα. Here, we report that B cell activation in nasal-associated lymphoid tissue (NALT) upon stimulation with the hapten (4-hydroxy-3-nitrophenyl)acetyl (NP) coupled to chicken γ globulin caused an anti-NP memory response dominated by high affinity IgA antibodies. In the response, however, NP-specific IgG+ B cells expanded and sustained their number as a major population in germinal centers (GCs), supporting the view that CSR to IgG heavy chain constant region, Cγ, operated efficiently in NALT. Both IgG+ and IgA+ GC B cells accumulated somatic mutations, indicative of affinity maturation to a similar extent, suggesting that both types of cell were equally selected by antigen. Despite the selection in GCs, high affinity NP-specific B cells were barely detected in the IgG memory compartment, whereas such cells dominated the IgA memory compartment. Taken together with the analysis of the VH gene clonotype in GC and memory B cells, we propose that NALT is equipped with a unique machinery providing IgA-specific enrichment of high affinity cells into the memory compartment, facilitating immunity with high affinity and noninflammatory secretory antibodies.

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5

Koni, Pandelakis A., and Richard A. Flavell. "Lymph Node Germinal Centers Form in the Absence of Follicular Dendritic Cell Networks." Journal of Experimental Medicine 189, no. 5 (March 1, 1999): 855–64. http://dx.doi.org/10.1084/jem.189.5.855.

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Follicular dendritic cell networks are said to be pivotal to both the formation of germinal centers (GCs) and their functions in generating antigen-specific antibody affinity maturation and B cell memory. We report that lymphotoxin β–deficient mice form GC cell clusters in the gross anatomical location expected of GCs, despite the complete absence of follicular dendritic cell networks. Furthermore, antigen-specific GC generation was at first relatively normal, but these GCs then rapidly regressed and GC-phase antibody affinity maturation was reduced. Lymphotoxin β–deficient mice also showed substantial B cell memory in their mesenteric lymph nodes. This memory antibody response was of relatively low affinity for antigen at week 4 after challenge, but by week 10 after challenge was comparable to wild-type, indicating that affinity maturation had failed in the GC phase but developed later.

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6

Torrellas, Josep, Andrew Tucker, and Anoop Gupta. "Benefits of cache-affinity scheduling in shared-memory multiprocessors." ACM SIGMETRICS Performance Evaluation Review 21, no. 1 (June 1993): 272–74. http://dx.doi.org/10.1145/166962.167038.

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7

Neuberger, Michael S., Michael R. Ehrenstein, Cristina Rada, Julian Sale, Facundo D. Batista, Gareth Williams, and Cesar Milstein. "Memory in the B–cell compartment: antibody affinity maturation." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, no. 1395 (March 29, 2000): 357–60. http://dx.doi.org/10.1098/rstb.2000.0573.

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In the humoral arm of the immune system, the memory response is not only more quickly elicited and of greater magnitude than the primary response, but it is also different in quality. In the recall response to antigen, the antibodies produced are of higher affinity and of different isotype (typically immunoglobulin G rather than immunoglobulin M). This maturation rests on the antigen dependence of B–cell maturation and is effected by programmed genetic modifications of the immunoglobulin gene loci. Here we consider how the B–cell response to antigen depends on the affinity of the antigen–receptor interaction. We also compare and draw parallels between the two processes, which underpin the generation of secondaryresponse antibodies: V gene somatic hypermutation and immunoglobulin heavy–chain class switching.

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8

Góes, Luís Fabrício Wanderley, Christiane Pousa Ribeiro, Márcio Castro, Jean-François Méhaut, Murray Cole, and Marcelo Cintra. "Automatic Skeleton-Driven Memory Affinity for Transactional Worklist Applications." International Journal of Parallel Programming 42, no. 2 (May 31, 2013): 365–82. http://dx.doi.org/10.1007/s10766-013-0253-x.

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9

Kaji, Tomohiro, Akiko Ishige, Masaki Hikida, Junko Taka, Atsushi Hijikata, Masato Kubo, Takeshi Nagashima, et al. "Distinct cellular pathways select germline-encoded and somatically mutated antibodies into immunological memory." Journal of Experimental Medicine 209, no. 11 (October 1, 2012): 2079–97. http://dx.doi.org/10.1084/jem.20120127.

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One component of memory in the antibody system is long-lived memory B cells selected for the expression of somatically mutated, high-affinity antibodies in the T cell–dependent germinal center (GC) reaction. A puzzling observation has been that the memory B cell compartment also contains cells expressing unmutated, low-affinity antibodies. Using conditional Bcl6 ablation, we demonstrate that these cells are generated through proliferative expansion early after immunization in a T cell–dependent but GC-independent manner. They soon become resting and long-lived and display a novel distinct gene expression signature which distinguishes memory B cells from other classes of B cells. GC-independent memory B cells are later joined by somatically mutated GC descendants at roughly equal proportions and these two types of memory cells efficiently generate adoptive secondary antibody responses. Deletion of T follicular helper (Tfh) cells significantly reduces the generation of mutated, but not unmutated, memory cells early on in the response. Thus, B cell memory is generated along two fundamentally distinct cellular differentiation pathways. One pathway is dedicated to the generation of high-affinity somatic antibody mutants, whereas the other preserves germ line antibody specificities and may prepare the organism for rapid responses to antigenic variants of the invading pathogen.

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10

Smith, Kenneth G. C., Amanda Light, Lorraine A. O'Reilly, Soon-Meng Ang, Andreas Strasser, and David Tarlinton. "bcl-2 Transgene Expression Inhibits Apoptosis in the Germinal Center and Reveals Differences in the Selection of Memory B Cells and Bone Marrow Antibody-Forming Cells." Journal of Experimental Medicine 191, no. 3 (February 7, 2000): 475–84. http://dx.doi.org/10.1084/jem.191.3.475.

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Immunization with T cell–dependent antigens generates long-lived memory B cells and antibody-forming cells (AFCs). Both populations originate in germinal centers and, predominantly, produce antibodies with high affinity for antigen. The means by which germinal center B cells are recruited into these populations remains unclear. We have examined affinity maturation of antigen-specific B cells in mice expressing the cell death inhibitor bcl-2 as a transgene. Such mice had reduced apoptosis in germinal centers and an excessive number of memory B cells with a low frequency of V gene somatic mutation, including those mutations encoding amino acid exchanges known to enhance affinity. Despite the frequency of AFCs being increased in bcl-2–transgenic mice, the fraction secreting high-affinity antibody in the bone marrow at day 42 remained unchanged compared with controls. The inability of BCL-2 to alter selection of bone marrow AFCs is consistent with these cells being selected within the germinal center on the basis of their affinity being above some threshold rather than their survival being due to a selective competition for an antigen-based signal. Continuous competition for antigen does, however, explain formation of the memory compartment.

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11

MacLennan, Ian C. M., Carola García de Vinuesa, and Montserrat Casamayor-Palleja. "B–cell memory and the persistence of antibody responses." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, no. 1395 (March 29, 2000): 345–50. http://dx.doi.org/10.1098/rstb.2000.0571.

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Antigens such as viral envelope proteins and bacterial exotoxins induce responses which result in the production of neutralizing antibody. These responses persist for years and provide highly efficient defence against reinfection. During these antibody responses a proportion of participating B cells mutate the genes that encode their immunoglobulin variable regions. This can increase the affinity of the antibody, but can also induce autoreactive B cells. Selection mechanisms operate which allow the cells with high affinity for the provoking antigen to persist, while other B cells recruited into the response die.

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12

Krummey, Scott M., Ryan J. Martinez, Rakieb Andargachew, Danya Liu, Maylene Wagener, Jacob E. Kohlmeier, Brian D. Evavold, Christian P. Larsen, and Mandy L. Ford. "Low-Affinity Memory CD8+ T Cells Mediate Robust Heterologous Immunity." Journal of Immunology 196, no. 6 (February 10, 2016): 2838–46. http://dx.doi.org/10.4049/jimmunol.1500639.

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13

Diener, Matthias, Eduardo H. M. Cruz, Marco A. Z. Alves, Philippe O. A. Navaux, Anselm Busse, and Hans-Ulrich Heiss. "Kernel-Based Thread and Data Mapping for Improved Memory Affinity." IEEE Transactions on Parallel and Distributed Systems 27, no. 9 (September 1, 2016): 2653–66. http://dx.doi.org/10.1109/tpds.2015.2504985.

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14

Karatza, Helen D. "Cache affinity and resequencing in a shared-memory multiprocessing system." Journal of Systems and Software 51, no. 1 (April 2000): 7–18. http://dx.doi.org/10.1016/s0164-1212(99)00104-1.

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15

Diener, Matthias, Eduardo H. M. Cruz, Marco A. Z. Alves, Philippe O. A. Navaux, and Israel Koren. "Affinity-Based Thread and Data Mapping in Shared Memory Systems." ACM Computing Surveys 49, no. 4 (February 6, 2017): 1–38. http://dx.doi.org/10.1145/3006385.

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16

Rieber, Robert W. "Hypnosis, false memory and multiple personality: a trinity of affinity." History of Psychiatry 10, no. 37 (March 1999): 003–11. http://dx.doi.org/10.1177/0957154x9901003701.

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17

Squillante, M. S., and E. D. Lazowska. "Using processor-cache affinity information in shared-memory multiprocessor scheduling." IEEE Transactions on Parallel and Distributed Systems 4, no. 2 (1993): 131–43. http://dx.doi.org/10.1109/71.207589.

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18

Markatos, E. P., and T. J. LeBlanc. "Using processor affinity in loop scheduling on shared-memory multiprocessors." IEEE Transactions on Parallel and Distributed Systems 5, no. 4 (April 1994): 379–400. http://dx.doi.org/10.1109/71.273046.

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19

Simon, Mitchell, Christopher Y. Ko, Sonya Baidar, Razvan L. Cornea, Julie Bossuyt, and Donald M. Bers. "Cardiac CAMKIIδ Memory: How Post-Translational-Modifications Alter Calmodulin Affinity." Biophysical Journal 118, no. 3 (February 2020): 35a. http://dx.doi.org/10.1016/j.bpj.2019.11.368.

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20

Vora, K. A., and T. Manser. "Altering the antibody repertoire via transgene homologous recombination: evidence for global and clone-autonomous regulation of antigen-driven B cell differentiation." Journal of Experimental Medicine 181, no. 1 (January 1, 1995): 271–81. http://dx.doi.org/10.1084/jem.181.1.271.

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Antibody VH transgenes containing small amounts of natural 5' and 3' flanking DNA undergo nonreciprocal homologous recombination with the endogenous Igh locus in B cells. The resulting "hybrid" heavy chain loci are generated at a low frequency but are fully functional, undergoing somatic hypermutation and isotype class switching. We have used this recombination pathway to introduce a somatically mutated variable (V) region with an unusually high affinity for the hapten p-azophenylarsonate (Ars) into the preimmune antibody repertoire. The affinity of this V region for Ars is 100-fold higher than any unmutated anti-Ars antibody previously characterized. Expression of the transgene-encoded V region did not affect many aspects of antigen-driven B cell differentiation, including somatic hypermutation, in either Ars-specific transgene- or endogenous V gene-expressing clones. Thus, the regulation of these processes appears to operate in a "global" fashion, in that the mechanisms involved are imperceptive of the relative affinities for antigen of the antibodies expressed by B cell clones participating in the immune response. In contrast, the selection of V region mutants leading to affinity maturation and memory cell formation was found to be strongly influenced by the transgenic V region, but only in clones expressing this V region. Hybridomas derived from transgene- and endogenous V region-expressing memory cells were isolated at similar frequencies from individual transgenic mice. The V regions expressed by hybridomas in both of these groups had 2- to 30-fold greater affinity for Ars than their unmutated precursors, despite the fact that the transgene-encoded precursors had 100-fold higher affinity than their endogenous counterparts. These results show that the criterion for entry into the memory compartment is established not by the affinity of a B cell's V region relative to all other V regions expressed during the response, but by the affinity of this V region relative to its unmutated precursor. Thus, the development of B cell memory is regulated in a "clone-autonomous" fashion.

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21

Savelyeva, Natalia, Michael Shipton, Amy Suchacki, Gavin Babbage, and Freda K. Stevenson. "High-affinity memory B cells induced by conjugate vaccines against weak tumor antigens are vulnerable to nonconjugated antigen." Blood 118, no. 3 (July 21, 2011): 650–59. http://dx.doi.org/10.1182/blood-2011-01-328864.

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Abstract Induction of antibody-mediated immunity against hematologic malignancies requires CD4+ T-cell help, but weak tumor antigens generally fail to induce adequate T-cell responses, or to overcome tolerance. Conjugate vaccines can harness alternative help to activate responses, but memory B cells may then be exposed to leaking tumor-derived antigen without CD4+ T-cell support. We showed previously using lymphoma-derived idiotypic antigen that exposure to “helpless” antigen silences the majority of memory IgG+ B cells. Transfer experiments now indicate that silencing is permanent. In marked contrast to IgG, most coexisting IgM+ memory B cells exposed to “helpless” antigen survive. Confirmation in a hapten (NP) model allowed measurement of affinity, revealing this, rather than isotype, as the determinant of survival. IgM+ B cells had Ig variable region gene usage similar to IgG but with fewer somatic mutations. Survival of memory B cells appears variably controlled by affinity for antigen, allowing a minority of low affinity IgG+, but most IgM+, memory B cells to escape deletion in the absence of T-cell help. The latter remain, but the majority fail to undergo isotype switch. These findings could apply to other tumor antigens and are relevant for vaccination strategies aimed to induce long-term antibody.

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22

Tokunaga, Akihiro, Daisuke Sugiyama, Yuka Maeda, Allison Betof Warner, Katherine S. Panageas, Sachiko Ito, Yosuke Togashi, Chika Sakai, Jedd D. Wolchok, and Hiroyoshi Nishikawa. "Selective inhibition of low-affinity memory CD8+ T cells by corticosteroids." Journal of Experimental Medicine 216, no. 12 (September 19, 2019): 2701–13. http://dx.doi.org/10.1084/jem.20190738.

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Patients treated with immune checkpoint blockade (ICB) sometimes experience immune-related adverse events (irAEs), requiring immuno-suppressive drugs such as corticosteroids despite the possibility that immunosuppression may impair the antitumor effects of ICB. Here, we address the dilemma of using corticosteroids for the treatment of irAEs induced by ICB. ICB augments neoantigen-specific CD8+ T cell responses, resulting in tumor regression. In our model, simultaneous, but not late, administration of corticosteroids impaired antitumor responses with reduction of CD8+ T cell proliferation. Secondary challenge using tumors with/without the neoantigen showed selective progression in tumors lacking the neoantigen when corticosteroids were administered. Corticosteroids decreased low- but not high-affinity memory T cells by suppressing fatty acid metabolism essential for memory T cells. In a small cohort of human melanoma patients, overall survival was shorter after treatment with CTLA-4 blockade in patients who received early corticosteroids or had low tumor mutation burden. Together, low-affinity memory T cells are dominantly suppressed by corticosteroids, necessitating careful and thoughtful corticosteroid use.

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23

Meffre, Eric, Nadia Catalan, Françoise Seltz, Alain Fischer, Michel C. Nussenzweig, and Anne Durandy. "Somatic Hypermutation Shapes the Antibody Repertoire of Memory B Cells in Humans." Journal of Experimental Medicine 194, no. 3 (August 6, 2001): 375–78. http://dx.doi.org/10.1084/jem.194.3.375.

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High-affinity antibodies produced by memory B cells differ from antibodies produced in naive B cells in two respects. First, many of these antibodies show somatic hypermutation, and second, the repertoire of antibodies expressed in memory responses is highly selected. To determine whether somatic hypermutation is responsible for the shift in the antibody repertoire during affinity maturation, we analyzed the immunoglobulin lambda light chain (Igλ) repertoire expressed by naive and antigen-selected memory B cells in humans. We found that the Igλ repertoire differs between naive and memory B cells and that this shift in the repertoire does not occur in the absence of somatic hypermutation in patients lacking activation-induced cytidine deaminase (AID). Our work suggests that somatic hypermutation makes a significant contribution to shaping the antigen-selected antibody repertoire in humans.

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24

Kulkarni, Rajan P. "Later is better: Corticosteroids selectively suppress early memory T cells." Science Translational Medicine 11, no. 513 (October 9, 2019): eaaz3711. http://dx.doi.org/10.1126/scitranslmed.aaz3711.

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25

Barrington, Robert A., Olga Pozdnyakova, Mohammad R. Zafari, Christopher D. Benjamin, and Michael C. Carroll. "B Lymphocyte Memory." Journal of Experimental Medicine 196, no. 9 (October 28, 2002): 1189–200. http://dx.doi.org/10.1084/jem.20021110.

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To dissect the influence of CD21/CD35 and FcγRIIB in antigen retention and humoral memory, we used an adoptive transfer model in which antigen-primed B and T lymphocytes were given to sublethally irradiated wild-type mice or mice deficient in CD21/CD35 (Cr2−/−) or FcγRIIB receptors (FcγRIIB−/−). Cr2−/− chimeras showed impaired memory as characterized by a decrease in antibody titer, reduced frequency of antibody secreting cells, an absence of affinity maturation, and significantly reduced recall response. The impaired memory in Cr2−/− chimeras corresponded with the reduced frequency of antigen-specific memory B cells. Interestingly, FcγRIIB−/− chimeras showed a differential phenotype with impaired splenic but normal bone marrow responses. These data suggest that CD21/CD35 on stroma, including follicular dendritic cells, is critical to the maintenance of long-term B lymphocyte memory.

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26

Notidis, Evangelia, Shailaja Hande, and Tim Manser. "Enforced Expression of Bcl-2 Selectively Perturbs Negative Selection of Dual Reactive Antibodies." Developmental Immunology 8, no. 3-4 (2001): 223–34. http://dx.doi.org/10.1155/2001/83595.

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We investigated the role of apoptosis in the development of B cell memory by analyzing the (p-azophenylarsonate) Ars response in a line of A strain mice in which expression of human Bcl-2 was enforced in the B cell compartment. Previous studies of the Ars immune response in these A. Bcl-2 mice, demonstrated that a large percentage of the antibodies expressed by the Ars induced memory B cell compartment had accumulated point mutations via somatic hypermutation that increased their affinity for both Ars and the autoantigen DNA (“dual reactive” antibodies). This was in sharp contrast to normal A strain mice which displayed no dual reactive B cells in their Ars induced memory B cell compartment. These data suggested that interference with apoptotic pathways regulated by Bcl-2 allows developing memory B cells that have acquired autoreactivity to bypass a peripheral tolerance checkpoint. Further studies of these mice, reported here, demonstrate that enforced expression of Bcl-2 does not alter serum antibody affinity maturation nor positive selection of B cells expressing somatically mutated antibody with an increased affinity for Ars. Moreover, the somatic hypermutation process was unaffected in A. Bcl-2 mice. Thus, enforced expression of Bcl-2 in A. Bcl-2 mice appears to selectively alter a negative selection process that operates during memory B cell differentiation.

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27

Frost, Elizabeth L., Anna E. Kersh, Brian D. Evavold, and Aron E. Lukacher. "Cutting Edge: Resident Memory CD8 T Cells Express High-Affinity TCRs." Journal of Immunology 195, no. 8 (September 14, 2015): 3520–24. http://dx.doi.org/10.4049/jimmunol.1501521.

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28

Solouki, Sabrina, Weishan Huang, Jessica Elmore, Candice Limper, Fei Huang, and Avery August. "TCR Signal Strength and Antigen Affinity Regulate CD8+ Memory T Cells." Journal of Immunology 205, no. 5 (August 5, 2020): 1217–27. http://dx.doi.org/10.4049/jimmunol.1901167.

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29

WANG, YI-MIN, and RUEI-CHUAN CHANG. "A MINIMAL SYNCHRONIZATION OVERHEAD AFFINITY SCHEDULING ALGORITHM FOR SHARED-MEMORY MULTIPROCESSORS." International Journal of High Speed Computing 07, no. 02 (June 1995): 231–49. http://dx.doi.org/10.1142/s0129053395000130.

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30

Torrellas, J., A. Tucker, and A. Gupta. "Evaluating the Performance of Cache-Affinity Scheduling in Shared-Memory Multiprocessors." Journal of Parallel and Distributed Computing 24, no. 2 (February 1995): 139–51. http://dx.doi.org/10.1006/jpdc.1995.1014.

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31

Wong, Rachel, Julia A. Belk, Jennifer Govero, Jennifer L. Uhrlaub, Dakota Reinartz, Haiyan Zhao, John M. Errico, et al. "Affinity-Restricted Memory B Cells Dominate Recall Responses to Heterologous Flaviviruses." Immunity 53, no. 5 (November 2020): 1078–94. http://dx.doi.org/10.1016/j.immuni.2020.09.001.

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32

Casson, L. P., and T. Manser. "Random mutagenesis of two complementarity determining region amino acids yields an unexpectedly high frequency of antibodies with increased affinity for both cognate antigen and autoantigen." Journal of Experimental Medicine 182, no. 3 (September 1, 1995): 743–50. http://dx.doi.org/10.1084/jem.182.3.743.

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To gain insight into the mechanism and limitations of antibody affinity maturation leading to memory B cell formation, we generated a phage display library of random mutants at heavy chain variable (V) complementarity determining region 2 positions 58 and 59 of an anti-p-azophenylarsonate (Ars) Fab. Single amino acid substitutions at these positions resulting from somatic hypermutation are recurrent products of affinity maturation in vivo. Most of the ex vivo mutants retained specificity for Ars. Among the many mutants displaying high Ars-binding activity, only one contained a position 58 and 59 amino acid combination that has been previously observed among the monoclonal antibodies (mAbs) derived from Ars-immunized mice. Affinity measurements on 14 of the ex vivo mutants with high Ars-binding activity showed that 11 had higher intrinsic affinities for Ars that the wild-type V region. However, nine of these Fabs also bound strongly to denatured DNA, a property neither displayed by the wild-type V region nor observed among the mutants characteristic of in vivo affinity maturation. These data suggest that ex vivo enhancement of mAb affinity via site-directed and random mutagenesis approaches may often lead to a reduction in antibody specificity that could complicate the use of the resulting mAbs for diagnostic and therapeutic applications. Moreover, the data are compatible with a hypothesis proposing that increased specificity for antigen, rather than affinity per se, is the driving force for formation of the memory B cell compartment.

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33

Blink, Elizabeth J., Amanda Light, Axel Kallies, Stephen L. Nutt, Philip D. Hodgkin, and David M. Tarlinton. "Early appearance of germinal center–derived memory B cells and plasma cells in blood after primary immunization." Journal of Experimental Medicine 201, no. 4 (February 14, 2005): 545–54. http://dx.doi.org/10.1084/jem.20042060.

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Immunization with a T cell–dependent antigen elicits production of specific memory B cells and antibody-secreting cells (ASCs). The kinetic and developmental relationships between these populations and the phenotypic forms they and their precursors may take remain unclear. Therefore, we examined the early stages of a primary immune response, focusing on the appearance of antigen-specific B cells in blood. Within 1 wk, antigen-specific B cells appear in the blood with either a memory phenotype or as immunoglobulin (Ig)G1 ASCs expressing blimp-1. The memory cells have mutated VH genes; respond to the chemokine CXCL13 but not CXCL12, suggesting recirculation to secondary lymphoid organs; uniformly express B220; show limited differentiation potential unless stimulated by antigen; and develop independently of blimp-1 expression. The antigen-specific IgG1 ASCs in blood show affinity maturation paralleling that of bone marrow ASCs, raising the possibility that this compartment is established directly by blood-borne ASCs. We find no evidence for a blimp-1–expressing preplasma memory compartment, suggesting germinal center output is restricted to ASCs and B220+ memory B cells, and this is sufficient to account for the process of affinity maturation.

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34

Paznikov, Alexey. "Optimization of thread affinity and memory affinity for remote core locking synchronization in multithreaded programs for multicore computer systems." Vibroengineering PROCEDIA 12 (June 30, 2017): 213–18. http://dx.doi.org/10.21595/vp.2017.18689.

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35

Baumgartner, Christina K., Hideo Yagita, and Laurent P. Malherbe. "A TCR Affinity Threshold Regulates Memory CD4 T Cell Differentiation following Vaccination." Journal of Immunology 189, no. 5 (July 27, 2012): 2309–17. http://dx.doi.org/10.4049/jimmunol.1200453.

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36

Eisen, Herman N. "Affinity Enhancement of Antibodies: How Low-Affinity Antibodies Produced Early in Immune Responses Are Followed by High-Affinity Antibodies Later and in Memory B-Cell Responses." Cancer Immunology Research 2, no. 5 (May 2014): 381–92. http://dx.doi.org/10.1158/2326-6066.cir-14-0029.

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37

Dal Porto, Joseph M., Ann M. Haberman, Garnett Kelsoe, and Mark J. Shlomchik. "Very Low Affinity B Cells Form Germinal Centers, Become Memory B Cells, and Participate in Secondary Immune Responses When Higher Affinity Competition Is Reduced." Journal of Experimental Medicine 195, no. 9 (May 6, 2002): 1215–21. http://dx.doi.org/10.1084/jem.20011550.

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To understand the relationship between the affinity of the B cell antigen receptor (BCR) and the immune response to antigen, two lines of immunoglobulin H chain transgenic (Tg) mice were created. H50Gμa and T1(V23)μa mice express μ H chain transgenes that associate with the λ1 L chains to bind the (4-hydroxy-3-nitrophenyl)acetyl hapten with association constants (Kas) of only 1.2 × 105 M−1 and 3 × 104 M−1, respectively. Both lines mounted substantial antibody-forming cell (AFC) and germinal center (GC) responses. H50Gμa Tg mice also generated memory B cells. T1(V23)μa B cells formed AFC and GCs, but were largely replaced in late GCs by antigen-specific cells that express endogenous BCRs. Thus, B lymphocytes carrying BCRs with affinities previously thought to be irrelevant in specific immune responses are in fact capable of complete T cell–dependent immune responses when relieved of substantial competition from other B cells. The failure to observe such B cells normally in late primary responses and in memory B cell populations is the result of competition, rather than an intrinsic inability of low affinity B cells.

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38

Stocum, David L., and Karen Crawford. "Use of retinoids to analyze the cellular basis of positional memory in regenerating amphibian limbs." Biochemistry and Cell Biology 65, no. 8 (August 1, 1987): 750–61. http://dx.doi.org/10.1139/o87-098.

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Cells of the amphibian limb regeneration blastema inherit memories of their level of origin (positional memory) along the limb axes. These memories serve as boundaries of what is to be regenerated, thus preventing regeneration of any but the missing structures. Because of its importance in determining the boundaries of regenerate pattern, it is essential to understand the cellular and molecular basis of positional memory. One approach to this problem is to look for position-related differences in a cell or molecular property along a limb axis and then show, using an agent that modifies regenerate pattern, that the cell or molecular property and the pattern are coordinately modified. We have done this using retinoic acid (RA) as a pattern-modifying agent and an in vivo assay that detects position-related differences in a cell recognition–affinity property along the proximodistal (PD) axis of the regenerating axolotl limb. RA proximalizes positional memory in the PD axis, posteriorizes it in the anteroposterior axis, and ventralizes it in the dorsoventral axis. The level-specific PD cell recognition–affinity property is proximalized by RA, indicating that this property and positional memory are causally related. The effects of RA on positional memory may be mediated through a cellular RA-binding protein (CRABP), since the concentration of unbound (apo) CRABP molecules is highest during early stages of regeneration when the proximalizing effects of RA are greatest.

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Quemeneur, Laurence, Veronique Angeli, Michael Chopin, and Rolf Jessberger. "SWAP-70 deficiency causes high-affinity plasma cell generation despite impaired germinal center formation." Blood 111, no. 5 (March 1, 2008): 2714–24. http://dx.doi.org/10.1182/blood-2007-07-102822.

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Germinal centers (GCs) are lymphoid tissue structures central to the generation of long-lived, high-affinity, antibody-forming B cells. However, induction, maintenance, and regulation of GCs are not sufficiently understood. The F-actin–binding, Rac-interacting protein SWAP-70 is strongly expressed in activated B cells like those in B follicles. Recent work suggests that SWAP-70 is involved in B-cell activation, migration, and homing. Therefore, we investigated the role of SWAP-70 in the T-dependent immune response, in GC formation, and in differentiation into plasma and memory B cells. Compared with wt, sheep red blood cell (SRBC)–, or NP-KLH–immunized SWAP-70−/− mice have strongly reduced numbers of GCs and GC-specific B cells. However, SWAP-70−/− NP-specific B cells accumulate outside of the B follicles, and SWAP-70−/− mice show more plasma cells in the red pulp and in the bone marrow, and increased NP-specific Ig and antibody-forming B cells. Yet the memory response is impaired. Thus, SWAP-70 deficiency uncouples GC formation from T-dependent antibody and long-lived plasma cell production and causes extrafollicular generation of high-affinity plasma cells, but does not adequately support the memory response.

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Wu, Hanchih, Ashley Witzl, and Hideki Ueno. "Assessment of TCR signal strength of antigen-specific memory CD8+ T cells in human blood." Blood Advances 3, no. 14 (July 18, 2019): 2153–63. http://dx.doi.org/10.1182/bloodadvances.2019000292.

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Abstract Assessment of the quality and the breadth of antigen (Ag)-specific memory T cells in human samples is of paramount importance to elucidate the pathogenesis and to develop new treatments in various diseases. T-cell receptor (TCR) signal strength, primarily controlled by TCR affinity, affects many fundamental aspects of T-cell biology; however, no current assays for detection of Ag-specific CD8+ T cells can assess their TCR signal strength in human samples. Here, we provide evidence that interferon regulatory factor 4 (IRF4), a transcription factor rapidly upregulated in correlation with TCR signal strength, permits the assessment of the TCR signal strength of Ag-specific CD8+ T cells in human peripheral blood mononuclear cells (PBMCs). Coexpression of IRF4 and CD137 sensitively detected peptide-specific CD8+ T cells with extremely low background in PBMCs stimulated for 18 hours with MHC class I peptides. Our assay revealed that human memory CD8+ T cells with high-affinity TCRs have an intrinsic ability to highly express CD25. Furthermore, HIV-specific CD8+ T cells in chronic HIV+ subjects were found to display primarily low-affinity TCRs with low CD25 expression capacity. Impairment in the functions of HIV-specific CD8+ T cells might be associated with their suboptimal TCR signals, as well as impaired responsiveness to interleukin-2.

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Köppert, Sebastian, Carla Wolf, Noémi Becza, Giuseppe A. Sautto, Fridolin Franke, Stefanie Kuerten, Ted M. Ross, Paul V. Lehmann, and Greg A. Kirchenbaum. "Affinity Tag Coating Enables Reliable Detection of Antigen-Specific B Cells in Immunospot Assays." Cells 10, no. 8 (July 21, 2021): 1843. http://dx.doi.org/10.3390/cells10081843.

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Assessment of humoral immunity to SARS-CoV-2 and other infectious agents is typically restricted to detecting antigen-specific antibodies in the serum. Rarely does immune monitoring entail assessment of the memory B-cell compartment itself, although it is these cells that engage in secondary antibody responses capable of mediating immune protection when pre-existing antibodies fail to prevent re-infection. There are few techniques that are capable of detecting rare antigen-specific B cells while also providing information regarding their relative abundance, class/subclass usage and functional affinity. In theory, the ELISPOT/FluoroSpot (collectively ImmunoSpot) assay platform is ideally suited for antigen-specific B-cell assessments since it provides this information at single-cell resolution for individual antibody-secreting cells (ASC). Here, we tested the hypothesis that antigen-coating efficiency could be universally improved across a diverse set of viral antigens if the standard direct (non-specific, low affinity) antigen absorption to the membrane was substituted by high-affinity capture. Specifically, we report an enhancement in assay sensitivity and a reduction in required protein concentrations through the capture of recombinant proteins via their encoded hexahistidine (6XHis) affinity tag. Affinity tag antigen coating enabled detection of SARS-CoV-2 Spike receptor binding domain (RBD)-reactive ASC, and also significantly improved assay performance using additional control antigens. Collectively, establishment of a universal antigen-coating approach streamlines characterization of the memory B-cell compartment after SARS-CoV-2 infection or COVID-19 vaccinations, and facilitates high-throughput immune-monitoring efforts of large donor cohorts in general.

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Fischer, Silke F., Philippe Bouillet, Kristy O'Donnell, Amanda Light, David M. Tarlinton, and Andreas Strasser. "Proapoptotic BH3-only protein Bim is essential for developmentally programmed death of germinal center-derived memory B cells and antibody-forming cells." Blood 110, no. 12 (December 1, 2007): 3978–84. http://dx.doi.org/10.1182/blood-2007-05-091306.

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Abstract T cell–dependent B-cell immune responses induce germinal centers that are sites for expansion, diversification, and selection of antigen-specific B cells. During the immune response, antigen-specific B cells are removed in a process that favors the retention of cells with improved affinity for antigen, a cell death process inhibited by excess Bcl-2. In this study, we examined the role of the BH3-only protein Bim, an initiator of apoptosis in the Bcl-2–regulated pathway, in the programmed cell death accompanying an immune response. After immunization, Bim-deficient mice showed persistence of both memory B cells lacking affinity-enhancing mutations in their immunoglobulin genes and antibody-forming cells secreting low-affinity antibodies. This was accompanied by enhanced survival of both cell types in culture. We have identified for the first time the physiologic mechanisms for killing low-affinity antibody-expressing B cells in an immune response and have shown this to be dependent on the BH3-only protein Bim.

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Kim, Sun Jung, Michele Caton, Chuansheng Wang, Magi Khalil, Zhi-Jie Zhou, John Hardin, and Betty Diamond. "Increased IL-12 inhibits B cells' differentiation to germinal center cells and promotes differentiation to short-lived plasmablasts." Journal of Experimental Medicine 205, no. 10 (September 22, 2008): 2437–48. http://dx.doi.org/10.1084/jem.20070731.

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B cells activated by antigen in T cell–dependent immune responses can become short-lived plasma cells, which remain in the spleen, or germinal center–derived memory or plasma cells, which show evidence of affinity maturation and, in the case of plasma cells, migrate to the bone marrow. We show that this cell fate decision can be governed by the cytokine environment engendered by activated dendritic cells (DCs). DCs from mice lacking the Fc receptor γ chain exhibited an activated phenotype in vitro. They secreted more of the proinflammatory cytokine IL-12, which led to the preferential generation of short-lived splenic plasma cells, with ensuing low affinity antibodies and a diminished recall response. Understanding the factors that regulate antigen-activated B cell differentiation and memory cell formation has implications for both antibody-mediated autoimmune disease and protective antibody responses.

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Vaswani, Raj, and John Zahorjan. "The implications of cache affinity on processor scheduling for multiprogrammed, shared memory multiprocessors." ACM SIGOPS Operating Systems Review 25, no. 5 (October 2, 1991): 26–40. http://dx.doi.org/10.1145/121133.121140.

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Pei, Zhao, Xiaoning Qi, Yanning Zhang, Miao Ma, and Yee-Hong Yang. "Human trajectory prediction in crowded scene using social-affinity Long Short-Term Memory." Pattern Recognition 93 (September 2019): 273–82. http://dx.doi.org/10.1016/j.patcog.2019.04.025.

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Viant, Charlotte, Georg H. J. Weymar, Amelia Escolano, Spencer Chen, Harald Hartweger, Melissa Cipolla, Anna Gazumyan, and Michel C. Nussenzweig. "Antibody Affinity Shapes the Choice between Memory and Germinal Center B Cell Fates." Cell 183, no. 5 (November 2020): 1298–311. http://dx.doi.org/10.1016/j.cell.2020.09.063.

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Nakagawa, Rinako, Amparo Toboso-Navasa, Marta Schips, George Young, Leena Bhaw-Rosun, Miriam Llorian-Sopena, Probir Chakravarty, et al. "Permissive selection followed by affinity-based proliferation of GC light zone B cells dictates cell fate and ensures clonal breadth." Proceedings of the National Academy of Sciences 118, no. 2 (January 8, 2021): e2016425118. http://dx.doi.org/10.1073/pnas.2016425118.

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Affinity maturation depends on how efficiently germinal centers (GCs) positively select B cells in the light zone (LZ). Positively selected GC B cells recirculate between LZs and dark zones (DZs) and ultimately differentiate into plasmablasts (PBs) and memory B cells (MBCs). Current understanding of the GC reaction presumes that cMyc-dependent positive selection of LZ B cells is a competitive affinity-dependent process; however, this cannot explain the production of GC-derived lower-affinity MBCs or retention of GC B cells with varied affinities. Here, by combining single-cell/bulk RNA sequencing and flow cytometry, we identified and characterized temporally and functionally distinct positively selected cMyc+ GC B cell subpopulations. cMyc+ LZ B cell subpopulations enriched with either higher- or lower-affinity cells diverged soon after permissive positive selection. The former subpopulation contained PB precursors, whereas the latter comprised less proliferative MBC precursors and future DZ entrants. The overall affinity of future DZ entrants was enhanced in the LZ through preferential proliferation of higher-affinity cells. Concurrently, lower-affinity cells were retained in GCs and protected from apoptosis. These findings redefine positive selection as a dynamic process generating three distinct B cell fates and elucidate how positive selection ensures clonal diversity for broad protection.

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48

Nakagawa, Rinako, Amparo Toboso-Navasa, Marta Schips, George Young, Leena Bhaw-Rosun, Miriam Llorian-Sopena, Probir Chakravarty, et al. "Permissive selection followed by affinity-based proliferation of GC light zone B cells dictates cell fate and ensures clonal breadth." Proceedings of the National Academy of Sciences 118, no. 2 (January 8, 2021): e2016425118. http://dx.doi.org/10.1073/pnas.2016425118.

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Affinity maturation depends on how efficiently germinal centers (GCs) positively select B cells in the light zone (LZ). Positively selected GC B cells recirculate between LZs and dark zones (DZs) and ultimately differentiate into plasmablasts (PBs) and memory B cells (MBCs). Current understanding of the GC reaction presumes that cMyc-dependent positive selection of LZ B cells is a competitive affinity-dependent process; however, this cannot explain the production of GC-derived lower-affinity MBCs or retention of GC B cells with varied affinities. Here, by combining single-cell/bulk RNA sequencing and flow cytometry, we identified and characterized temporally and functionally distinct positively selected cMyc+ GC B cell subpopulations. cMyc+ LZ B cell subpopulations enriched with either higher- or lower-affinity cells diverged soon after permissive positive selection. The former subpopulation contained PB precursors, whereas the latter comprised less proliferative MBC precursors and future DZ entrants. The overall affinity of future DZ entrants was enhanced in the LZ through preferential proliferation of higher-affinity cells. Concurrently, lower-affinity cells were retained in GCs and protected from apoptosis. These findings redefine positive selection as a dynamic process generating three distinct B cell fates and elucidate how positive selection ensures clonal diversity for broad protection.

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AGUILAR, JOSE, and ERNST LEISS. "PARALLEL LOOP SCHEDULING APPROACHES FOR DISTRIBUTED AND SHARED MEMORY SYSTEMS." Parallel Processing Letters 15, no. 01n02 (March 2005): 131–52. http://dx.doi.org/10.1142/s0129626405002118.

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In this paper, we propose different approaches for the parallel loop scheduling problem on distributed as well as shared memory systems. Specifically, we propose adaptive loop scheduling models in order to achieve load balancing, low runtime scheduling, low synchronization overhead and low communication overhead. Our models are based on an adaptive determination of the chunk size and an exploitation of the processor affinity property, and consider different situations (central or local queues, and dynamic or static loop partition).

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Siracusa, Francesco, Mairi A. McGrath, Patrick Maschmeyer, Markus Bardua, Katrin Lehmann, Gitta Heinz, Pawel Durek, et al. "Nonfollicular reactivation of bone marrow resident memory CD4 T cells in immune clusters of the bone marrow." Proceedings of the National Academy of Sciences 115, no. 6 (January 22, 2018): 1334–39. http://dx.doi.org/10.1073/pnas.1715618115.

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The bone marrow maintains memory CD4 T cells, which provide memory to systemic antigens. Here we demonstrate that memory CD4 T cells are reactivated by antigen in the bone marrow. In a secondary immune response, antigen-specific T cells of the bone marrow mobilize and aggregate in immune clusters together with MHC class II-expressing cells, mostly B lymphocytes. They proliferate vigorously and express effector cytokines, but they do not develop into follicular T-helper cells. Neither do the B lymphocytes develop into germinal center B cells in the bone marrow. Within 10 days, the immune clusters disappear again. Within 30 days, the expanded antigen-specific memory CD4 T cells return to memory niches and are maintained again individually as resting cells. Thus, in secondary immune responses in the bone marrow T-cell memory is amplified, while in germinal center reactions of secondary lymphoid organs humoral memory is adapted by affinity maturation.

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