Maintenance of memory CTL responses by T helper cells and CD40‐CD40 ligand: antibodies provide the key

Bachmann, Martin F.; Hunziker, Lukas; Zinkernagel, Rolf M.; Storni, Tazio; Köpf, Manfred

doi:10.1002/eji.200324717

Cited by 64 publications

(25 citation statements)

References 49 publications

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“…Moreover, observations that patients with Bruton's agammaglobulinemia can control acute viral diseases [22] helped create a generally held notion that, unlike what applies for protection against reinfection, primary viral infections were predominantly controlled by cell-mediated immunity [22]. Experiments in mice, monkeys, and man had shown that passive administration of potent nAbs or transgenic expression of a virus-neutralizing B cell receptor (BCR) can prevent infection [23,24], augment virus control during infection [25–27], or prevent the establishment of persistence [28,29]. Still, these experimental observations did not challenge the above dogma since the experimental conditions chosen did not mimic the kinetics and magnitude of the host's spontaneous nAb response (delayed and weak).…”

Section: Introductionmentioning

confidence: 99%

Impaired Antibody Response Causes Persistence of Prototypic T Cell–Contained Virus

et al. 2009

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CD8 T cells are recognized key players in control of persistent virus infections, but increasing evidence suggests that assistance from other immune mediators is also needed. Here, we investigated whether specific antibody responses contribute to control of lymphocytic choriomeningitis virus (LCMV), a prototypic mouse model of systemic persistent infection. Mice expressing transgenic B cell receptors of LCMV-unrelated specificity, and mice unable to produce soluble immunoglobulin M (IgM) exhibited protracted viremia or failed to resolve LCMV. Virus control depended on immunoglobulin class switch, but neither on complement cascades nor on Fc receptor γ chain or Fc γ receptor IIB. Cessation of viremia concurred with the emergence of viral envelope-specific antibodies, rather than with neutralizing serum activity, and even early nonneutralizing IgM impeded viral persistence. This important role for virus-specific antibodies may be similarly underappreciated in other primarily T cell–controlled infections such as HIV and hepatitis C virus, and we suggest this contribution of antibodies be given consideration in future strategies for vaccination and immunotherapy.

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Section: Introductionmentioning

confidence: 99%

Impaired Antibody Response Causes Persistence of Prototypic T Cell–Contained Virus

et al. 2009

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“…One study showed that CD4 + T cells are required after the priming and expansion phase (i.e., during the contraction phase) and that this help can be antigen non-specific 60 . CD4 + T cell help following LCMV infection is independent of CD40-mediated licensing of DCs or CD8 + T cells, with passive transfer of LCMV-specific antibodies sufficient to restore a protective memory CD8 + T cell response in the absence of CD40-CD40L interactions through the facilitation of viral clearance 62,63 . “Helpless” CD8 + T cells displayed increased expression of T-bet, a transcription factor involved in fine-tuning CD8 + effector and memory T cell differentiation, with reduction of T-bet expression restoring the functionality of these cells 64,65 .…”

Section: Cd4+ T Cell Help Following Systemic Infectionmentioning

confidence: 99%

The multifaceted role of CD4+ T cells in CD8+ T cell memory

2016

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Following infection, T cells differentiate into a heterogeneous population of effector T cells that can mediate pathogen clearance. A subset of these effector T cells possesses the ability to survive long-term and mature into memory T cells capable of providing long-term immunity. Understanding the signals that regulate the development of memory T cells is crucial to efforts to design vaccines capable of eliciting T cell-based immunity. CD4+ T cells are essential for the formation of protective memory CD8+ T cells following infection or immunization. However, until recently, the mechanisms by which CD4+ T cells act to support memory CD8+ T cell development following infection were unclear. Here, we discuss recent studies that provide insight into the multifaceted role of CD4+ T cells in the regulation of memory CD8+ T cell differentiation.

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“…But limited researches were reported on the genetic factors which influence the genesis of asymptomatic chronic HBV infections. Previous studies have demonstrated that activation of CD40 signaling is indispensable for the induction of effective virus-specific CD8+ T-cell responses, which is required for the virus clearance [30,31]. Using a transgenic mouse model, Chisari et al showed that the HBV antigen-specific CD8+ T cell exhaustion was able to be rescued by CD40-mediated mDC activation [32].…”

Section: Discussionmentioning

confidence: 99%

Association of CD40 -1C/T Polymorphism in the 5′-Untranslated Region with Chronic HBV Infection

Zhou

Jin

Tang

et al. 2015

Cell Physiol Biochem

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Background: CD40 is an important costimulatory molecule in both celluar and humoral immune responses, involved in the pathogenic processes of chronic inflammatory diseases. Few studies were performed on the association of CD40 single nucleotide polymorphism (SNP) with chronic hepatitis B virus (HBV) infection. In this study, we studied whether the CD40-1C/T polymorphism had any effect on the progression of chronic HBV infection in Chinese population. Methods: CD40 -1C/T polymorphism in the 5′-untranslated region was analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 453 chronic HBV carriers, who were divided into asymptomatic HBV carriers (ASC), moderate chronic hepatitis B group (MCHB) and severe chronic hepatitis B group (SCHB). 202 healthy individuals in the same region were enrolled in this study as the controls. The CD40 expression on B lymphocytes was detected by flow cytometry. The concentrations of soluble CD40 (sCD40) in sera were assayed by a commercial ELISA kit. Results: Our results showed the frequencies of TT genotype and T allele of CD40-1C/T polymorphism were higher significantly in ASC than those in controls (P< 0.05), while this result was not found in either MCHB or SCHB. On the surface of B lymphocytes, the CD40 expression levels in the individuals with TT genotype were significantly lower than those with CC and CT genotypes in either ASC group or healthy controls (P<0.001). The sCD40 levels in the sera of ASC, MCHB and SCHB groups were significantly higher than the controls (P<0.001). Conclusions: The CD40 -1C/T polymorphism may contribute to the susceptibility of asymptomatic HBV carriers through its effect on cell-surface CD40 expression, which indicated CD40 signaling was involved in immune tolerance of chronic HBV infection.

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Maintenance of memory CTL responses by T helper cells and CD40‐CD40 ligand: antibodies provide the key

Cited by 64 publications

References 49 publications

Impaired Antibody Response Causes Persistence of Prototypic T Cell–Contained Virus

Impaired Antibody Response Causes Persistence of Prototypic T Cell–Contained Virus

The multifaceted role of CD4+ T cells in CD8+ T cell memory

Association of CD40 -1C/T Polymorphism in the 5′-Untranslated Region with Chronic HBV Infection

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