CD4 monoclonal antibody pairs for immunosuppression and tolerance induction

Qin, Shixin; Cobbold, Stephen; Tighe, Helen; Benjamin, Richard J.; Waldmann, Herman

doi:10.1002/eji.1830170813

Cited by 166 publications

(94 citation statements)

References 35 publications

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“…with 1 mg of each of two synergistic mAb YTS 191.1.2 and YTA 3.1.2 [47]. Used mAb conjugates anti-CD8-Cy-Chrome, anti-CD44-biotin, anti-Annexin V-biotin, allophycocyaninstreptavidin and anti-IFN-c-allophycocyanin were purchased from BD Pharmingen.…”

Section: Antibodiesmentioning

confidence: 99%

Altered primary CD8⁺ T cell response to a modified virus Ankara(MVA)‐vectored vaccine in the absence of CD4⁺ T cell help

Estcourt¹,

McMichael²,

Hanke³

2005

Eur J Immunol

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T cell receptor-transgenic F5 mice were used to assess primary CD8 + T cell responses to a modified virus Ankara (MVA)-vectored vaccine in the absence of CD4 + T cell help. Naive, CD8-enriched, CFSE-labelled F5 cells were transferred into normal or CD4 + celldepleted mice and the mice were vaccinated with MVA.HIVA-NP. At different time points during the primary response, F5 cells were re-isolated and analysed on divisional basis for a number of parameters. We demonstrated that the primary CD8 + T cell response in the absence of CD4 + T cell help differed from that in normal CD4 + cellundepleted mice. While in the absence of CD4 + T cell help, the initial migratory progress from the local response to a systemic one was not grossly affected, the proportion of dying F5 cells during the expansion phase was markedly increased and resulted in an overall smaller expansion and significantly decreased frequency of CD8 + T cell memory after contraction. T cells primed without help displayed accelerated proliferation and activation, while expression of interferon-c remained similar. These phenomena were observed in the lymph nodes draining the MVA.HIVA-NP immunization site and were similar, but delayed by 2-3 days in spleen and non-draining lymph nodes. IntroductionCD8 + T cells form an important part of the immune defence against many intracellular pathogens including viruses. Historically, CD8 + T cell responses against viral infections were considered to be independent from 'help' provided by CD4 + T cells. This was explained by direct activation of antigen-presenting DC by viruses, which provided ligands for Toll-like receptors and proinflammatory signals [1][2][3]. Recently, this view was revised by studies of non-inflammatory antigens which suggested that while primary CD8 + T cell response was CD4 + T cell-independent, secondary CD8 + T cell response, i.e. development of functional memory, was dependent on CD4 + T cell help during priming. These data led to the formulation of a programming model [4][5][6]. In contrast, another set of recent studies pointed towards an environmental model and proposed that CD4 + T cells were required to enhance survival of fully functional memory CD8 + T cells rather than imparting essential programming during the primary response [7,8]. The differences in these conclusions may be explained by the use of different antigens and immunization protocols, which might lead to differential activation of DC. Collectively, these and other experiments [9][10][11][12][13] not required for triggering the CD8 + T cell program of multiple cell divisions, effector function maturation and cell number contraction, but was needed for differentiation into functional CD8 + T cell memory and/or its maintenance.To date, most studies investigated secondary responses to make conclusions about the dependence of the CD8 + T cell responses on CD4 help. This is partially because induction of a good memory is the ultimate aim of a successful vaccination, but also because primary CD8 + T cell responses to non-inf...

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Section: Antibodiesmentioning

confidence: 99%

Altered primary CD8⁺ T cell response to a modified virus Ankara(MVA)‐vectored vaccine in the absence of CD4⁺ T cell help

Estcourt¹,

McMichael²,

Hanke³

2005

Eur J Immunol

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“…The YTA3.1.2 hybridoma producing an IgG2b rat antimouse depleting CD4 monoclonal antibody (YTA3.1) 27 was a kind gift from Professor Herman Waldmann (Sir William Dunn School of Pathology, University of Oxford). The antibody was grown as ascites in (LOU × DA) F1 rats and purified by ammonium sulphate precipitation followed by DEAE Sephacel ion exchange chromatography.…”

Section: Anti-cd4 Pretreatmentmentioning

confidence: 99%

Adenoviral transfer of a single donor-specific MHC class I gene to recipient bone marrow cells can induce specific immunological unresponsiveness in vivo

2002

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“…6,8 Isolation of inflammatory cells from brain Collagenase digestion of the brain followed by isolation of the inflammatory cells using a density gradient has been previously described by Kajiwara et al 9 Flow cytometry Cells were incubated with 10% mouse serum for 15 min at 4°C before adding the primary antibodies for 45 min at 4°C. Rat anti-mouse primary antibodies were used as follows: TIB 122 (CD45), 68 KT3 (CD3), 69 YTA 3.1 (CD4), 70 and YTS 169.4 (CD8). 71 Cells were washed twice and then incubated with fluorescein (FITC) conjugated anti-rat IgG (Vector, Burlingame, CA, USA) for 45 min at 4°C.…”

Section: Adenoviral Vectorsmentioning

confidence: 99%

Variation in the immune response to adenoviral vectors in the brain: influence of mouse strain, environmental conditions and priming

et al. 1999

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E1-deleted adenoviral vectors expressing the bacterial ␤-ently made higher antibody responses than C57BL/6J galactosidase gene were inoculated into the brain of mice. Although adenoviral vectors induced an inflammatory unprimed and primed C3H.He or C57BL/6J mice housed response under all conditions, mice housed in SPF faciliunder either conventional or specific-pathogen-free (SPF) ties exhibited less inflammation than conventional mice conditions. The kinetics of immune responses to both the and transgene expression persisted for longer. Irrespective vector and the transgene were investigated. In mice preof whether the mice had been deliberately primed to adenviously sensitized to adenovirus, the leukocyte infiltrate in ovirus, antibody titres were consistently lower in SPF mice the brain was dominated by CD8 + T cells, whereas in compared with conventional mice. This study clearly demunprimed mice CD4 + T cells were present at higher levels.onstrates that environmental conditions, as well as preAs expected, antibody titres to both adenovirus and ␤-vious priming to adenovirus, will affect both the quality and galactosidase were higher in primed mice than in unprimed duration of the immune response triggered by gene mice after intracranial inoculation. C3H.He mice consistdelivery to the brain.

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CD4 monoclonal antibody pairs for immunosuppression and tolerance induction

Cited by 166 publications

References 35 publications

Altered primary CD8⁺ T cell response to a modified virus Ankara(MVA)‐vectored vaccine in the absence of CD4⁺ T cell help

Altered primary CD8⁺ T cell response to a modified virus Ankara(MVA)‐vectored vaccine in the absence of CD4⁺ T cell help

Adenoviral transfer of a single donor-specific MHC class I gene to recipient bone marrow cells can induce specific immunological unresponsiveness in vivo

Variation in the immune response to adenoviral vectors in the brain: influence of mouse strain, environmental conditions and priming

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CD4 monoclonal antibody pairs for immunosuppression and tolerance induction

Cited by 166 publications

References 35 publications

Altered primary CD8+ T cell response to a modified virus Ankara(MVA)‐vectored vaccine in the absence of CD4+ T cell help

Altered primary CD8+ T cell response to a modified virus Ankara(MVA)‐vectored vaccine in the absence of CD4+ T cell help

Adenoviral transfer of a single donor-specific MHC class I gene to recipient bone marrow cells can induce specific immunological unresponsiveness in vivo

Variation in the immune response to adenoviral vectors in the brain: influence of mouse strain, environmental conditions and priming

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Altered primary CD8⁺ T cell response to a modified virus Ankara(MVA)‐vectored vaccine in the absence of CD4⁺ T cell help

Altered primary CD8⁺ T cell response to a modified virus Ankara(MVA)‐vectored vaccine in the absence of CD4⁺ T cell help