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Affinity maturation of antibody responses is mediated by differential plasma cell proliferation

ABSTRACT: Affinity maturation of antibody responses is mediated by differential plasma cell proliferation

PROVIDER: PRJNA1188058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31395662.fastq.gz	Fastqsanger.gz
	SRR31395663.fastq.gz	Fastqsanger.gz
	SRR31395664.fastq.gz	Fastqsanger.gz
	SRR31395665.fastq.gz	Fastqsanger.gz
	SRR31395666.fastq.gz	Fastqsanger.gz

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Affinity maturation of antibody responses is mediated by differential plasma cell proliferation

Project description:Increased antibody affinity over time after vaccination is a prototypical feature of immune responses. Recent studies have shown that a diverse collection of B cells, producing antibodies with a wide spectrum of different affinities, are selected into the plasma cell (PC) pathway. How affinity-permissive selection enables PC affinity maturation remains unknown. Here we report that PC precursors (prePC) expressing high affinity antibodies received higher levels of T follicular helper (Tfh) and divided at higher rates than their lower affinity counterparts once they left the GC. Thus, differential cell division by selected prePCs accounted for how diverse precursors developed into a PC compartment that mediated serological affinity maturation.

2024-12-19 | GSE282284 | GEO

Regulated somatic hypermutation enhances antibody affinity maturation

Project description:Regulated somatic hypermutation enhances antibody affinity maturation

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Affinity maturation of antibody against membrane-bound GPCR molecules

Project description:Affinity maturation of antibody against membrane-bound GPCR molecules

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PRMT1 is required for antibody affinity maturation by preventing premature B cell differentiation

Project description:Germinal center (GC) B cells undergo cycles of somatic hypermutation and selection, thus increasing their antibody affinity before differentiating into plasma or memory cells. The mechanisms dictating the dynamics of GC B cells are incompletely understood. We show that ablating the Protein arginine methyltransferase 1 (PRMT1) in GC B cells reduces antibody affinity maturation by impairing GC dynamics, as shown by compromised GC expansion, accumulation of CXCR4- B cells, and increased memory B cell differentiation, partly, at the expense of plasma cell production. Furthermore, PRMT1 distinguishes the subset of GC B cells that reenter the GC dark zone after positive selection, in which it is upregulated by Myc in conjunction with mTORC signaling. PRMT1 opposes mature B cell differentiation, as shown by higher plasma cell differentiation of PRMT1-deficient B cells activated ex vivo, a function co-opted by B cell lymphoma cells, in which PRMT1 expression also correlates with Myc expression and outcome.

2023-04-27 | GSE189276 | GEO

Role of affinity in plasma cell development in the germinal center light zone

Project description:Protective immune responses to many pathogens depend on the development of high affinity antibody-producing plasma cells in germinal centers. Transgenic models suggest that there is a stringent affinity-based barrier to plasma cell development. Whether a similar high affinity barrier regulates plasma cell development under physiologic circumstances, and the nature of the plasma cell fate decision has not been defined precisely. Here we use a fate mapping approach to examine the relationship between germinal center (GC) B cells selected to undergo additional rounds of affinity maturation, germinal center pre-plasma cells and plasma cells. The data show that initial plasma cell selection overlaps with germinal center B cell selection, but that the plasma cell compartment accumulates a less diverse and higher affinity collection of antibodies over time. Thus, whereas the GC continues to diversify over time, affinity-based pre-plasma cell selection sieves the germinal center to enable accumulation of a more restricted group of high affinity antibody secreting plasma cells.

2023-11-02 | GSE246382 | GEO

Regulated somatic hypermutation enhances antibody affinity maturation

Project description:Germinal centers (GCs) are microenvironments where B cells undergo affinity maturation through somatic hypermutation (SHM) and selection by T follicular helper (TFH) cells. While SHM introduces mutations at a fixed rate (~1x10⁻³ per base pair per division), most mutations are deleterious, particularly in high-affinity B cells undergoing many divisions. This study tests a theoretical model suggesting that high-affinity B cells optimize maturation by dividing more but mutating less per division. Data from mice immunized with SARS-CoV-2 or a model antigen support the model, showing that high-affinity B cells shorten their G0/G1 phases and reduce mutation rates, safeguarding their lineages and improving affinity maturation outcomes.

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IRF4 Haploinsufficiency Impairs Affinity Maturation

Project description:IRF4 Haploinsufficiency Impairs Affinity Maturation

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PRMT1 is required for antibody affinity maturation by preventing premature B cell differentiation

Project description:PRMT1 is required for antibody affinity maturation by preventing premature B cell differentiation

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Affinity maturation broadens influenza vaccine-induced antibody responses in humans [bcr]

Project description:Influenza virus vaccination remains the best strategy for combating virus infection, but vaccine efficacy is highly variable. An ideal influenza vaccine must have two attributes: one, it should be capable of inducing broadly cross-reactive antibodies that can neutralize diverse influenza virus strains; and two, it must induce long-lived antibody responses to maintain protective immunity for extended periods. Germinal center (GC) reactions are the major sites where diversification and affinity maturation of B cells occur. Whether a persistent GC response could expand the breadth of responding B cell clones following influenza vaccination in humans remains unknown. Here, we show that influenza virus vaccine-specific GC B cells persist for over nine weeks post vaccination in two out of seven individuals. These late vaccine-specific GC B cells exhibited increased somatic hypermutation (SHM) of their B cell receptors compared to early vaccine-specific GC B cells. After re-immunization with seasonal influenza virus vaccine, individuals with a persistent GC engaged vaccine-specific plasmablasts (PBs) with higher SHM frequency. Tracking the maturation of three clonally related GC B cell lineages over time revealed that late GC B cells had receptors that recognized and neutralized heterologous influenza virus strains. Thus, SHM induced by persistent GCs can broaden the antibody response to influenza virus vaccination. This indicates that seasonal influenza virus vaccination in humans can induce broadly cross-reactive antibodies that target diverse influenza virus strains.

2024-06-13 | GSE211869 | GEO

Affinity maturation broadens influenza vaccine-induced antibody responses in humans [gex]

2024-06-13 | GSE211865 | GEO