Responses of CD27+CD38+ plasmablasts, and CD24hiCD27hi and CD24hiCD38hi regulatory B cells during primary dengue virus 2 infection

Lei, Chenshuang; Yu, Qinhua; Wang, Hong; Jie-jing, Liu; Chen, Sufeng; Zhao, Zhao; Qiu, Liannv

doi:10.1002/jcla.24035

Cited by 4 publications

(2 citation statements)

References 30 publications

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“…Chemokine receptor CXCR3+ expression has been associated with Type 1 T helper immune responses (Th1) (Sánchez-Vargas and Mathew, 2019; Sandberg et al, 2021; White et al, 2021). Moreover, PD-1 and ICOS expression is associated with B cell interaction in order to induce B cell activation (Lei et al, 2021; Shi et al, 2018). This analysis was performed only on groups CD4+/DENV2/CD4+/ZIKV, CD4-/DENV2/CD4+/ZIKV and CD4+/DENV2/CD8-/ZIKV because they have CD4+ T cell populations before ZIKV infection.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, PD-1 and ICOS expression is associated with B cell interaction in order to induce B cell activation (Lei et al, 2021;Shi et al, 2018). This analysis was performed only on groups CD4+/DENV2/CD4+/ZIKV, CD4-/DENV2/CD4+/ZIKV and CD4+/DENV2/CD8-/ZIKV because they have CD4+ T cell populations before ZIKV infection.…”

Section: Cd4 + Peripheral T Helper Cells (Ptfh) Are Present In Circul...mentioning

confidence: 99%

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CD4+ T Cell Depletion Before Primary Dengue and/or Secondary Zika Infection Reveals Mechanistic Correlates of Antibody Functionality in Rhesus Macaques

Serrano-Collazo,

Miranda,

Cruz

et al. 2024

Preprint

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Dengue (DENV) virus and Zika virus (ZIKV) are two flaviviruses of major public health concern. One drawback designing effective vaccines is our limited understanding of the mechanisms ruling protection or harm among DENV serotypes, or between DENV and ZIKV. Here, we depleted rhesus macaques of CD4+T cellsin vivobefore primary DENV infection and/or secondary ZIKV challenge to recreate a sub-optimal priming of the humoral immune response. Our results support that CD4+T cells are needed to induce a quantitative and type-specific effective humoral immune response against primary DENV, but also against secondary ZIKV in DENV-experimented subjects. Our results also indicate a limited contribution of the DENV-Memory B cells to anti-ZIKV response. Furthermore, our results suggest that a suboptimal B cell priming during a primary DENV infection does differentially impact different antibody (Abs) properties. While binding or neutralization of ZIKV or DENV during a subsequent exposure to ZIKV is not affected by the lack of CD4+T - B cells interaction during a primary DENV infection, that interaction is critical to guarantee the Abs specificity. Also, we found that depleting CD4+T cells before DENV primary infection but not before ZIKV challenge significantly increases Abs cross-reactivity against DENV-EDIII domain and DENV-NS1 protein but not against ZIKV-EDIII domain or NS1 protein. Furthermore, there was more cross-reactivity among the DENV-NS1 proteins than against DENV-EDIII domains, suggesting that during a primary DENV infection CD4+T cells have a different weight in the responses against EDIII domain and NS1 protein. The proper Abs binding and neutralization with increased cross-reactivity profile was associated with limited frequency of circulating peripheral T helper cells (pTfh) with T helper 1 phenotype (CD4+/CXCR5+/CXCR3+) and expressing markers related to B cell activation (CXCR5+/CXCR3+/PD-1+/ICOS+) in the group depleted of CD4+T cells only before primary DENV infection. However, memory B cells – but not Antibody Secreting Cells (ASC) activation 7 days after the infection – positively correlate with those two populations of pTfh. Finally, when Abs cross-reactivity values were incorporated in a Principal Component Analysis (PCA), the DENV-CD4+T depleted group separates from the other two groups with similar Abs binding and neutralization profiles. Our result strongly suggests that during a heterologous sequential DENV/ZIKV infections Abs binding, and neutralization, may be regulated by different factors than their specificity. Before, the induction of cross-neutralizing Abs has been described in the context of secondary DENV infection. Here, for the first time, we are reproducing the experimental conditions leading to the generation of such Abs populationin vivo. In summary, we show that suboptimal immune priming during a primary flavivirus infection has functional consequences during a secondary heterologous infection. These results have huge implications understanding the immune response to DENV vaccines (and maybe ZIKV), including why an optimal vaccine or natural-induced neutralizing response not necessarily protects or enhances pathogenesis during a subsequent natural heterologous exposure.

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Section: Resultsmentioning

confidence: 99%

Section: Cd4 + Peripheral T Helper Cells (Ptfh) Are Present In Circul...mentioning

confidence: 99%

CD4+ T Cell Depletion Before Primary Dengue and/or Secondary Zika Infection Reveals Mechanistic Correlates of Antibody Functionality in Rhesus Macaques

Serrano-Collazo,

Miranda,

Cruz

et al. 2024

Preprint

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Responses of CD27⁺CD38⁺ plasmablasts, and CD24^hiCD27^hi and CD24^hiCD38^hi regulatory B cells during primary dengue virus 2 infection

Lei

Wang

et al. 2021

Clinical Laboratory Analysis

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Dengue fever, a highly infectious disease transmitted by Aedes mosquitoes, is caused by four serotypes of dengue virus (DENV), which has led to 400 million infections annually in over 100 countries. 1 Most infections are subclinical; however, in some cases, DENV infection results in a variety of clinical symptoms, ranging from mild fever (dengue fever) to dengue shock syndrome and dengue hemorrhagic fever, which is fatal. 2,3 Currently, no approved antiviral drugs are available to treat DENV infection; therefore, the only management option for patients is symptomatic treatment. 4,5 DENV infection induces the expansion of memory B cells and plasmablasts. [6][7][8][9][10] Plasmablasts further differentiate into antibodysecreting plasma cells associated with an antigen-specific B-cell

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Immunomodulation in dengue: towards deciphering dengue severity markers

Dash,

Samal,

Rout

et al. 2024

Cell Commun Signal

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Background Dengue is a vector-borne debilitating disease that is manifested as mild dengue fever, dengue with warning signs, and severe dengue. Dengue infection provokes a collective immune response; in particular, the innate immune response plays a key role in primary infection and adaptive immunity during secondary infection. In this review, we comprehensively walk through the various markers of immune response against dengue pathogenesis and outcome. Main body Innate immune response against dengue involves a collective response through the expression of proinflammatory cytokines, such as tumor necrosis factors (TNFs), interferons (IFNs), and interleukins (ILs), in addition to anti-inflammatory cytokines and toll-like receptors (TLRs) in modulating viral pathogenesis. Monocytes, dendritic cells (DCs), and mast cells are the primary innate immune cells initially infected by DENV. Such immune cells modulate the expression of various markers, which can influence disease severity by aiding virus entry and proinflammatory responses. Adaptive immune response is mainly aided by B and T lymphocytes, which stimulate the formation of germinal centers for plasmablast development and antibody production. Such antibodies are serotype-dependent and can aid in virus entry during secondary infection, mediated through a different serotype, such as in antibody-dependent enhancement (ADE), leading to DENV severity. The entire immunological repertoire is exhibited differently depending on the immune status of the individual. Short conclusion Dengue fever through severe dengue proceeds along with the modulated expression of several immune markers. In particular, TLR2, TNF-α, IFN-I, IL-6, IL-8, IL-17 and IL-10, in addition to intermediate monocytes (CD14+CD16+) and Th17 (CD4+IL-17+) cells are highly expressed during severe dengue. Such markers could assist greatly in severity assessment, prompt diagnosis, and treatment.

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Responses of CD27⁺CD38⁺ plasmablasts, and CD24^hiCD27^hi and CD24^hiCD38^hi regulatory B cells during primary dengue virus 2 infection

Cited by 4 publications

References 30 publications

CD4+ T Cell Depletion Before Primary Dengue and/or Secondary Zika Infection Reveals Mechanistic Correlates of Antibody Functionality in Rhesus Macaques

CD4+ T Cell Depletion Before Primary Dengue and/or Secondary Zika Infection Reveals Mechanistic Correlates of Antibody Functionality in Rhesus Macaques

Responses of CD27⁺CD38⁺ plasmablasts, and CD24^hiCD27^hi and CD24^hiCD38^hi regulatory B cells during primary dengue virus 2 infection

Immunomodulation in dengue: towards deciphering dengue severity markers

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