Anti-CD25 Antibody Enhancement of Vaccine-Induced Immunogenicity: Increased Durable Cellular Immunity with Reduced Immunodominance

Moore, Anne; Gallimore, Awen; Draper, Simon J.; Watkins, K; Gilbert, Sarah C.; Hill, Adrian V. S.

doi:10.4049/jimmunol.175.11.7264

Cited by 88 publications

(73 citation statements)

References 49 publications

(51 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[18][19][20][21] IL 5 The induction or expansion of Tregs could be considered a drawback to vaccination strategies within certain settings, and the ability of IL-28B to influence this subpopulation of CD4 ϩ T cells has not previously been studied. As IL-28B falls into the same IFN family as IL-29, we addressed the possibility that it may exert similar effects on the Treg cell population.…”

Section: Il-28b But Not Il-12 Increases Hiv Gag-specific Igg2amentioning

confidence: 99%

“…This result is consistent with a previous report describing a similar change in Treg populations after vaccination. 20 Inclusion of cytokine adjuvants in vaccination dramatically altered Treg populations in various fashions. Interestingly, the use of IL-12 as an immunoadjuvant significantly increased the number of splenic Tregs in immunized mice compared with mice vaccinated with the HIV Gag4Y construct alone ( Figure 5B).…”

Section: Il-28b But Not Il-12 Increases Hiv Gag-specific Igg2amentioning

confidence: 99%

See 1 more Smart Citation

Comparative ability of IL-12 and IL-28B to regulate Treg populations and enhance adaptive cellular immunity

Morrow

Pankhong

Laddy

et al. 2009

Blood

137

107

View full text Add to dashboard Cite

Improving the potency of immune responses is paramount among issues concerning vaccines against deadly pathogens. IL-28B belongs to the newly described interferon lambda (IFN) family of cytokines, and has not yet been assessed for its potential ability to influence adaptive immune responses or act as a vaccine adjuvant. We compared the ability of plasmid-encoded IL-28B to boost immune responses to a multiclade consensus HIV Gag plasmid during DNA vaccination with that of IL-12. We show here that IL-28B, like IL-12, is capable of robustly enhancing adaptive immunity. Moreover, we describe for the first time how IL-28B reduces regulatory T-cell populations during DNA vaccination, whereas IL-12 increases this cellular subset. We also show that IL-28B, unlike IL-12, is able to increase the percentage of splenic CD8 ؉ T cells in vaccinated animals, and that these cells are more granular and have higher antigen-specific cytolytic degranulation compared with cells taken from animals that received IL-12 as an adjuvant. Lastly, we report that IL-28B can induce 100% protection from mortality after a lethal influenza challenge. These data suggest that IL-28B is a strong candidate for further studies of vaccine or immunotherapy protocols. (Blood. 2009;113:5868-5877)

show abstract

Section: Il-28b But Not Il-12 Increases Hiv Gag-specific Igg2amentioning

confidence: 99%

Section: Il-28b But Not Il-12 Increases Hiv Gag-specific Igg2amentioning

confidence: 99%

Comparative ability of IL-12 and IL-28B to regulate Treg populations and enhance adaptive cellular immunity

Morrow

Pankhong

Laddy

et al. 2009

Blood

137

107

View full text Add to dashboard Cite

show abstract

“…Similarly, new knowledge of the role of CD4 + , CD25 + , FOX-P3 + regulatory T cells in both controlling HIV-1 and other vaccine responses [204] and the role of adjuvants in regulation both the production in the thymus and peripheral proliferation of regulatory T cells [PEACOCK J, HAYNES BF, SEMPOWSKI G, MANUSCRIPT SUBMITTED], have also enabled of design of new formulations of adjuvants and vaccines for induction and maintenance of the desired immune responses.…”

Section: Adjuvant Design For Hiv-1 Vaccinesmentioning

confidence: 99%

Aiming to induce broadly reactive neutralizing antibody responses with HIV-1 vaccine candidates

Haynes¹,

Montefiori²

2006

Expert Review of Vaccines

103

View full text Add to dashboard Cite

Neutralizing antibody induction is a key feature of many effective vaccines and is the only immune response that has proven to be capable of completely blocking AIDS virus infection in animal models. Unfortunately, the extensive genetic variability and complex immune-evasion strategies of HIV-1 have thwarted all attempts to date at eliciting an effective neutralizing antibody response with candidate HIV-1 vaccine immunogens. Recent advances in our understanding of how these evasion strategies operate, coupled with growing progress in unravelling the structure and immunobiology of the viral envelope glycoproteins, are contributing to novel immunogen designs to overcome the many barriers to inducing protective antibodies against HIV-1. Keywordsantiretroviral therapy; HIV-1; host cell fusion; immunogen; neutralizing antibody induction Development of a safe, practical and effective HIV-1 vaccine is one of the highest priorities of the global scientific community [1,2]. Although antiretroviral therapy (ART) has dramatically prolonged the lives of HIV-1 infected patients, ART is not yet routinely available in developing countries, and the global rate of spread of HIV-1 continues unabated. If no effective AIDS vaccine is developed by 2010, the number of people infected world-wide with HIV-1 could exceed 60 million [3].In spite of more than 20 years of research, the types of immune responses needed to protect an immunized individual from HIV-1 infection are not known. Its is known that CD8 + cytotoxic T-cell responses can control HIV-1 replication to varying degrees in acute HIV-1 infection (AHI) [4,5], and when induced by immunogens, can control viral set point after simian immunodeficiancy virus (SIV) or simian HIV (SHIV) challenges in non-human primates [4]. Strong proliferative CD4 + T-cell responses to HIV-1 proteins have been demonstrated to correlate well with immune control of HIV-1 viral load [5]. Therefore, it is highly desirable for an HIV-1 vaccine co induce robust CD4 + and CD8 + T-cell responses in order to control virus replication and reduce the likelihood of subsequent transmission [4][5][6][7]. The potential for complete ('sterilizing') immunity from HIV-1 infection may depend on the presence of pre-existing neutralizing antibodies. We know that neutralizing antibodies can prevent the acquisition of AIDS virus infection after intravenous, vaginal, rectal and oral virus challenge in nonhuman primates [8][9][10][11][12]. This level of protection is highly attractive for a vaccine against a virus, such as HIV-1, which integrates genetically and forms latent viral reservoirs soon after infection. However, the diversity of transmitted HIV-1 genetic variants and the relative resistance of the majority of HIV-1 primary isolates to most types of inducible neutralizing antibodies have posed major hurdles to current vaccine efforts. Furthermore, the few rare broadly reactive neutralizing monoclonal antibodies (mAbs) that have been isolated from HIV-1 infected patients represent species of antibodies that...

show abstract

“…ϩ constitutively expressing CD4 ϩ T cells, and regulatory cells (4,17,19,25,28,30). Binding of anti-CD25 antibody to the IL-2␣ receptors of both effector and regulatory cells would limit their proliferation (34).…”

Section: Fig 5 Borreliacidal Antibody Titers Ofmentioning

confidence: 99%

Anti-CD25 Antibody Treatment of Mice Vaccinated and Challenged withBorreliaspp. Does Not Exacerbate Arthritis but Inhibits Borreliacidal Antibody Production

Nardelli

Warner

Callister

et al. 2006

Clin Vaccine Immunol

View full text Add to dashboard Cite

CD4؉ CD25 ؉ T cells are a population of regulatory T cells responsible for the modulation of the immune response in several autoimmune and infectious disease models. We previously showed that adoptive transfer of enriched CD4 ؉ CD25 ؉ T cells also plays a major role in the prevention of arthritis in Borrelia-vaccinated (Borrelia burgdorferi isolate 297) and -challenged (B. bissettii) mice. Here, we present evidence that administration of anti-CD25 antibody at the time of challenge or at later intervals fails to enhance the development of severe destructive osteoarthropathy in Borrelia-vaccinated C57BL mice. However, Borrelia-vaccinated and -challenged mice receiving anti-CD25 antibody developed decreased borreliacidal antibody titers compared to vaccinated and challenged controls. These findings suggest that additional mechanisms besides CD4 ؉ CD25 ؉ T cells are involved in the regulation of the immune response to Borrelia infection following vaccination.We showed previously that severe destructive arthritis could be induced in Borrelia-vaccinated and -challenged mice (6, 9, 33, 34). The arthritis was prevented when these mice were treated with anti-interleukin 17 (IL-17) antibody (6). Concomitantly, the anti-IL-17-treated Borrelia-vaccinated and -challenged mice developed an inordinate number of CD4 ϩ CD25 ϩ T cells in the lymph nodes adjacent to the arthritic site (33). When anti-IL-17-treated Borrelia-vaccinated and -challenged mice were administered anti-CD25 antibody, the number of CD4 ϩ CD25 ϩ T cells decreased. More importantly, severe destructive arthritis was induced (33). These results suggest that CD4 ϩ CD25 ϩ T cells play an important role in the prevention of arthritis.The importance of CD4 ϩ CD25 ϩ T cells in prevention of arthritis was further advanced by adoptive transfer studies (34). Highly purified CD4 ϩ CD25 ϩ T cells were obtained from Borrelia-vaccinated and -infected mice treated with anti-IL-17 antibody. When Borrelia-vaccinated and -challenged mice were infused with CD4 ϩ CD25 ϩ T cells, they failed to develop severe destructive arthritis. In contrast, Borrelia-vaccinated and -challenged recipients of CD4 ϩ CD25 Ϫ T cells developed inflammation of the subsynovial tissues surrounding the tibiotarsal joint, destruction of articular cartilage, synovial hyperplasia, and infiltration of neutrophils into the synovial space. Together, these approaches establish that CD4 ϩ CD25 ϩ T cells can act to control the immunopathology of arthritis.It is clear that CD4 ϩ CD25 ϩ T cells are essential for maintaining homeostasis of the immune system (1, 48), especially for control of autoimmune diseases (3,16, 37, 38,(43)(44)(45). In addition, the regulatory activity of these naturally occurring CD4ϩ CD25 ϩ T cells can be modulated by antigen stimulation or exposure to various cytokines (7, 13). Treatment of Borreliavaccinated and -challenged mice with anti-IL-17 antibody may have altered the immune system to produce a unique and potent population of CD4 ϩ CD25 ϩ cells that prevent arthritis (33). Here, we ...

show abstract

Anti-CD25 Antibody Enhancement of Vaccine-Induced Immunogenicity: Increased Durable Cellular Immunity with Reduced Immunodominance

Cited by 88 publications

References 49 publications

Comparative ability of IL-12 and IL-28B to regulate Treg populations and enhance adaptive cellular immunity

Comparative ability of IL-12 and IL-28B to regulate Treg populations and enhance adaptive cellular immunity

Aiming to induce broadly reactive neutralizing antibody responses with HIV-1 vaccine candidates

Anti-CD25 Antibody Treatment of Mice Vaccinated and Challenged withBorreliaspp. Does Not Exacerbate Arthritis but Inhibits Borreliacidal Antibody Production

Contact Info

Product

Resources

About