From dendritic cells to B cells dysfunctions during <scp>HIV</scp>‐1 infection: T follicular helper cells at the crossroads

Ruffin, Nicolas; Hani, Lylia; Seddiki, Nabila

doi:10.1111/imm.12730

Cited by 6 publications

(2 citation statements)

References 101 publications

(277 reference statements)

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“…T FH cells are the key CD4 + memory subset that drives B cell activation and differentiation through both soluble (IL-4 and IL-21) and cognate (CD40 ligand) interactions. As activated memory CD4 + cells, T FH cells may be the preferential targets of HIV-1 infection in germinal centers (45), where they are increased, rather than decreased, in number with HIV-1 infection (19, 46, 47). Increased numbers of circulating T FH are associated with development of broadly neutralizing antibodies against HIV-1(48).…”

Section: Discussionmentioning

confidence: 99%

Effective B cell activation in vitro during viremic HIV-1 infection with surrogate T cell stimulation

et al. 2018

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Identifying HIV-1-associated B cell defects and responses to activation may direct interventions to circumvent their impaired antibody responses to infection and vaccines. Among 34 viremic HIV-1-infected and 20 seronegative control adults, we measured baseline frequencies and activation of B and T cell subsets, expression of activation-induced cytidine deaminase (AID), potential determinants of B cell activation in vivo and B and T cell responses in vitro. At baseline, HIV-1 infection was associated with increased IgM memory and decreased anergic cell frequencies, as well as increased activation in all 10 B cell subsets compared with controls. HIV-1 status, T activation, and BAFF were significant potential drivers of B cell activation. Despite high baseline activation among HIV-1-infected subjects, stimulation in vitro with combined surrogates for antigen (anti-IgM), cognate (CD40 ligand) and soluble T cell factors (IL-4) elicited comparable B cell activation, transitions from naïve to class-switched memory cells and AID expression in both groups. In summary, viremic HIV-1 infection perturbs circulating B cell subsets and activation at each stage of B cell maturation. However, that appropriate stimulation of B cells elicits effective activation and maturation provides impetus for advancing vaccine development to prevent secondary infections by circumventing early B cell defects.

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Section: Discussionmentioning

confidence: 99%

Effective B cell activation in vitro during viremic HIV-1 infection with surrogate T cell stimulation

et al. 2018

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“…HCV uses dendritic cell-specific intercellular adhesion molecule 3-grabbing non-integrin, the major receptor present on DCs, to enter the DCs and thus uses these cells as reservoirs 40 . There are many reports which suggest that DCs lose their functions in terms of their maturation capacity and antigen presentation, in patients infected with CHC 41 42 . The expression levels of co-stimulatory molecules (CD80 and CD86) and MHC class II molecules (HLA-DR and HLA-DQ) are lowered in patients infected with CHC as compared to normal volunteers 43 .…”

Section: Dendritic Cells (Dcs)mentioning

confidence: 99%

A juggernaut of innate & adaptive immune cells in chronic hepatitis C

Tomer

Arora

2020

Indian Journal of Medical Research

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Hepatitis C virus (HCV) is a small positive-sense, single-stranded RNA virus, the causal organism for chronic hepatitis. Chronic hepatitis leads to inflammation of liver, causing cirrhosis, fibrosis and steatosis, which may ultimately lead to liver cancer in a few cases. Innate and adaptive immune responses play an important role in the pathogenesis of HCV infection, thus acting as an important component in deciding the fate of the disease. Numerous studies have indicated that the derangement of these immune responses results in the persistence of infection leading to chronic state of the disease. Interactions between virus and host immune system generally result in the elimination of virus, but as the virus evolves with different evading mechanisms, it makes environment favourable for its survival and replication. It has been reported that HCV impairs the immune system by functional modulation of the cells of innate as well as adaptive immune responses, resulting in chronic state of the disease, influencing the response to antiviral therapy in these patients. These defects in the immune system lead to suboptimal immune responses and therefore, impaired effector functions. This review highlights the involvement or association of different immune cells such as natural killer cells, B cells, dendritic cells and T cells in HCV infection and how the virus plays a role in manipulating certain regulatory mechanisms to make these cells dysfunctional for its own persistence and survival.

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Co-Infection with TB and HIV: Converging Epidemics, Clinical Challenges, and Microbial Synergy

Huante

Nusbaum

Endsley

2019

Tuberculosis Host-Pathogen Interactions

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From dendritic cells to B cells dysfunctions during HIV‐1 infection: T follicular helper cells at the crossroads

Cited by 6 publications

References 101 publications

Effective B cell activation in vitro during viremic HIV-1 infection with surrogate T cell stimulation

Effective B cell activation in vitro during viremic HIV-1 infection with surrogate T cell stimulation

A juggernaut of innate & adaptive immune cells in chronic hepatitis C

Co-Infection with TB and HIV: Converging Epidemics, Clinical Challenges, and Microbial Synergy

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