scholarly journals Higher levels of B‐cell mutation in the early germinal centres of an inefficient secondary antibody response to a variant influenza haemagglutinin

Immunology ◽  
2019 ◽  
Vol 157 (1) ◽  
pp. 86-91
Author(s):  
Richard K. Tennant ◽  
Barbara Holzer ◽  
John Love ◽  
Elma Tchilian ◽  
Harry N. White
Keyword(s):  
Antibody Response ◽  
B Cell ◽  
Secondary Antibody ◽  
Germinal Centres ◽  
Cell Mutation

scholarly journals CELL-TO-CELL INTERACTION IN THE IMMUNE RESPONSE

1971 ◽  
Vol 134 (1) ◽  
pp. 66-82 ◽  
Author(s):  
J. F. A. P. Miller ◽  
J. Sprent
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Antibody Response ◽  
B Cell ◽  
Cell Population ◽  
Thoracic Duct ◽  
Secondary Antibody ◽  
Cba Mice ◽  
Duct Cells

Collaboration between thymus-derived lymphocytes and nonthymus-derived antibody-forming cell precursors occurs in the primary antibody response of mice to heterologous erythrocytes and serum proteins. The purpose of the experiments reported here was to determine whether collaboration took place in an adoptive secondary antibody response. A chimeric population of lymphocytes was produced by reconstituting neonatally thymectomized CBA mice soon after birth with (CBA x C57BL)F1 thymus lymphocytes. These mice could be effectively primed to fowl immunoglobulin G (FγG) and their thoracic duct lymphocytes adoptively transferred memory responses to irradiated mice. The activity of these cells was impaired markedly by preincubation with CBA anti-C57BL serum and to a lesser extent by anti-θ-serum. Reversal of this deficiency was obtained by adding T cells in the form of thoracic duct cells from normal CBA mice. Cells from FγG-primed mice were at least 10 times as effective as cells from normal mice or from CBA mice primed to horse erythrocytes. These results were considered to support the concept that memory resides in the T cell population and that collaboration between T and B cells is necessary for an optimal secondary antibody response. Poor antibody responses were obtained in irradiated mice given mixtures of thoracic duct cells from primed mice and of B cells from unprimed mice (in the form of spleen or thoracic duct cells from thymectomized donors). In contrast to the situation with T cells, the deficiency in the B cell population could not be reversed by adding B cells from unprimed mice. It was considered that memory resides in B cells as well as in T cells and that priming probably entails a change in the B cell population which is fundamentally different from that produced in the T cell population.

scholarly journals In vitro analysis of allogeneic lymphocyte interaction. I. Characterization and cellular origin of an Ia-positive helper factor- allogeneic effect factor

1977 ◽  
Vol 146 (4) ◽  
pp. 1019-1032 ◽  
Author(s):  
TL Delovitch ◽  
HO McDevitt
Keyword(s):  
T Cell ◽  
B Cells ◽  
Antibody Response ◽  
B Cell ◽  
Cell Population ◽  
Cell Function ◽  
Mouse Strains ◽  
Secondary Antibody ◽  
Effect Factor ◽  
Ia Antigens

A soluble allogeneic effect factor (AEF) was produced by using H-2 congenic mouse strains and a serum.free cell culture medium. An AEF derived from untreated activated responder cells and irradiated stimulator cells provided helper cell function in a primary and secondary antibody response for both T-cell-depleted responder B cells and stimulator B cells. This interaction may be determined by genes situated in the I-A and I-B regions: additional K-region control was not excluded. Ia antigens, but neither H-2 nor Ig determinants are molecular constituents of AEF. The active components of this AEF consist, in part, of Ia antigens derived from both the activated responder cell population and irradiated stimulator cell population. An AEF derived from Ia negative responder cells and irradiated T-cell- depleted stimulator cells helps a secondary antibody response of T-cell- depleted stimulator B cells but not responder B cells. This genetically restricted AEF contains Ia antigens determined by the stimulator haplotype but not the responder haplotype. The priming antigen, DNP- keyhole limpet hemocyanin, is not a component of restricted AEF. The data suggest that restricted AEF may be a product of a stimulator B cell and/or macrophage. They support the hypothesis that the recognition by allogeneic T cells of Ia antigens on B cells activates the B cell to IgG antibody production.

scholarly journals Cell-to-cell interaction controlled by immunoglobulin genes. Role of Thy-1-, Lyt-1+, Ig+ (B') cell in allotype-restricted antibody production.

1982 ◽  
Vol 156 (2) ◽  
pp. 443-453 ◽  
Author(s):  
K Okumura ◽  
K Hayakawa ◽  
T Tada
Keyword(s):  
T Cells ◽  
B Cells ◽  
Antibody Response ◽  
B Cell ◽  
Antibody Production ◽  
Helper T Cells ◽  
Secondary Antibody ◽  
T And B Cells ◽  
Athymic Nude Mice

A novel lymphocyte subpopulation, designated "B' cell" because of its characteristic dual expression of Ig and Lyt-1 antigen, is described in relation to its ability to augment the in vitro secondary antibody response. The cells are found in the spleens of normal unprimed mice as well as those of athymic nude mice and represent a small of normal unprimed mice as well as those of athymic nude mice and represent a small number (2-3%) of immunoglobulin-positive cells. No other distinguishing surface markers of conventional T and B cells, such as Thy-1, Lyt-2, Ia, and ThB antigens, are detected on the B' cell. In the in vitro anti-hapten secondary antibody response, the addition of a small number of B' cells from unprimed mice to the mixture of T and B cells greatly augmented the anti-hapten antibody formation when the number of carrier-specific helper T cells was limited. This augmentation was observed only when B and B' cells shared the same set of IgVH genes. The identity of the immunoglobulin gene between T cells and B or B' cells was not necessary for optimum antibody production. The results indicate that the presence of B' cells is necessary for the induction of an optimum antibody response when helper T cells are limited. It is suggested that B' cells deliver an additional signal to the B cell network to magnify the antibody response.

Regulation of the in vitro secondary antibody response

1980 ◽  
Vol 55 (2) ◽  
pp. 302-311 ◽  
Author(s):  
Sharyn M. Walker ◽  
William O. Weigle
Keyword(s):  
Antibody Response ◽  
Secondary Antibody

scholarly journals IMMUNOLOGIC TOLERANCE AFTER SPECIFIC IMMUNIZATION

1964 ◽  
Vol 120 (3) ◽  
pp. 435-447 ◽  
Author(s):  
Marianne M. Dorner ◽  
Jonathan W. Uhr
Keyword(s):  
Human Serum Albumin ◽  
Bovine Serum Albumin ◽  
Antibody Response ◽  
Serum Albumin ◽  
Human Serum ◽  
Bovine Serum ◽  
The State ◽  
Immunologic Tolerance ◽  
Secondary Antibody

Specific immunologic tolerance to bovine serum albumin (BSA) was induced in approximately one-half of the rabbits that had been primarily immunized and were prepared for a secondary antibody response to BSA. The state of tolerance lasted for several months in the majority of rabbits and was not easily terminated by immunization with human serum albumin followed by BSA.

scholarly journals A highly specific antibody response after protein prime-peptide boost immunization with Eppin/B-cell epitope in mice

2011 ◽  
Vol 7 (8) ◽  
pp. 849-855 ◽  
Author(s):  
Zhengqiong Chen ◽  
Wei He ◽  
Yuzhang Wu ◽  
Ping Yan ◽  
Haiyang He ◽  
...  
Keyword(s):  
Antibody Response ◽  
B Cell ◽  
Specific Antibody ◽  
Cell Epitope ◽  
Specific Antibody Response ◽  
B Cell Epitope ◽  
Boost Immunization

scholarly journals SARS-CoV-2 infection severity is linked to superior humoral immunity against the spike

2020 ◽  
Author(s):  
Jenna J. Guthmiller ◽  
Olivia Stovicek ◽  
Jiaolong Wang ◽  
Siriruk Changrob ◽  
Lei Li ◽  
...  
Keyword(s):  
Antibody Response ◽  
B Cell ◽  
Cell Response ◽  
Nucleocapsid Protein ◽  
Antigen Specificity ◽  
Memory B Cell ◽  
Reading Frame ◽  
Global Pandemic ◽  
Kinetics Of ◽  
B Cell Response

ABSTRACTSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently causing a global pandemic. The antigen specificity and kinetics of the antibody response mounted against this novel virus are not understood in detail. Here, we report that subjects with a more severe SARS-CoV-2 infection exhibit a larger antibody response against the spike and nucleocapsid protein and epitope spreading to subdominant viral antigens, such as open reading frame 8 and non-structural proteins. Subjects with a greater antibody response mounted a larger memory B cell response against the spike, but not the nucleocapsid protein. Additionally, we revealed that antibodies against the spike are still capable of binding the D614G spike mutant and cross-react with the SARS-CoV-1 receptor binding domain. Together, this study reveals that subjects with a more severe SARS-CoV-2 infection exhibit a greater overall antibody response to the spike and nucleocapsid protein and a larger memory B cell response against the spike.

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