Antigen Presenting B Cells Facilitate CD4 T Cell Cooperation Resulting in Enhanced Generation of Effector and Memory CD4 T Cells

Kroeger, David R.; Rudulier, Christopher D.; Bretscher, Peter A.

doi:10.1371/journal.pone.0077346

Cited by 21 publications

(30 citation statements)

References 40 publications

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“…Irradiated mice similarly reconstituted with the same number of syngeneic spleen cells, but immunized with a 10-fold lower dose of OVA-SRBC, barely generated a detectable response, and the presence of the additional DO11.10 transgenic cells resulted in a substantial and predominant Th1 response. This is in line with previous findings that CD4 T cell cooperation can facilitate the activation of Th1 cells (37)(38)(39). Importantly, increasing the number of DO11.10 cells transferred with a low dose of Ag once again facilitated the development of a Th2 anti-SRBC response (Fig.…”

Section: Resultssupporting

confidence: 92%

The Number of Responding CD4 T Cells and the Dose of Antigen Conjointly Determine the Th1/Th2 Phenotype by Modulating B7/CD28 Interactions

Rudulier

McKinstry

Al‐Yassin

et al. 2014

The Journal of Immunology

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Our previous in vivo studies show that both the amount of Ag and the number of available naive CD4 T cells affect the Th1/Th2 phenotype of the effector CD4 T cells generated. We examined how the number of OVA-specific CD4 TCR transgenic T cells affects the Th1/Th2 phenotype of anti-SRBC CD4 T cells generated in vivo upon immunization with different amounts of OVA-SRBC. Our observations show that a greater number of Ag-dependent CD4 T cell interactions are required to generate Th2 than Th1 cells. We established an in vitro system that recapitulates our main in vivo findings to more readily analyze the underlying mechanism. The in vitro generation of Th2 cells depends, as in vivo, upon both the number of responding CD4 T cells and the amount of Ag. We demonstrate, using agonostic/antagonistic Abs to various costimulatory molecules or their receptors, that the greater number of CD4 T cell interactions, required to generate Th2 over Th1 cells, does not involve CD40, OX40, or ICOS costimulation, but does involve B7/CD28 interactions. A comparison of the level of expression of B7 molecules by APC and CD4 T cells, under different conditions resulting in the substantial generation of Th1 and Th2 cells, leads us to propose that the critical CD28/B7 interactions, required to generate Th2 cells, may directly occur between CD4 T cells engaged with the same B cell acting as an APC.

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Section: Resultssupporting

confidence: 92%

The Number of Responding CD4 T Cells and the Dose of Antigen Conjointly Determine the Th1/Th2 Phenotype by Modulating B7/CD28 Interactions

Rudulier

McKinstry

Al‐Yassin

et al. 2014

The Journal of Immunology

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“…The 1999 model for CD4 T cell activation postulated that the Ag-specific cooperation between Q-specific and R-specific CD4 T cells would be mediated by a B cell specific for either Q or R, able to take up the conjugate Ag via its Ag-specific receptors. Our studies support such a role for B cells in mediating CD4 T cell cooperation (48,49).…”

Section: Observations and Concepts On The Importance Of The Role Of Bsupporting

confidence: 79%

Does T Cell Activation Require a Quorum of Lymphocytes?

Al‐Yassin

Bretscher

2018

The Journal of Immunology

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Recent reports suggest a quorum of T cells is required to activate T lymphocytes and that this requirement may help explain why scarce lymphocytes, specific for peripheral self-antigen, are rarely activated by Ag. This proposal runs counter to the commonly held framework that the Ag-dependent, but CD4 T lymphocyte–independent, activation of CD8 T lymphocytes, and the activation of CD4 T lymphocytes themselves, can occur when a single CD8 or CD4 T lymphocyte encounters Ag under appropriately dangerous circumstances. We argue that a review of older literature often ignored, as well as of contemporary studies, supports the quorum concept and is difficult to reconcile with the Danger Model.

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“…Without cosignaling from T‐cells, B‐cells differentiate into short‐lived plasma cells and these generally are the B‐cells found in the marginal zone and mucosa . As mentioned earlier, B‐cells are also capable of Ag presentation to T‐cells by expressing MHC II molecules with bound peptide, and these lymphocyte–lymphocyte interactions have been suggested to influence the fate of both types of lymphocytes and to shape immune outcomes …”

Section: Deconstructing the Immune Microenvironment Of Lymphoid Tissuesmentioning

confidence: 94%

Deconstructing Immune Microenvironments of Lymphoid Tissues for Reverse Engineering

Witzel¹,

Nasser

Garcia-Sabaté

et al. 2018

Adv Healthcare Materials

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The immune microenvironment presents a diverse panel of cues that impacts immune cell migration, organization, differentiation, and the immune response. Uniquely, both the liquid and solid phases of every specific immune niche within the body play an important role in defining cellular functions in immunity at that particular location. The in vivo immune microenvironment consists of biomechanical and biochemical signals including their gradients, surface topography, dimensionality, modes of ligand presentation, and cell–cell interactions, and the ability to recreate these immune biointerfaces in vitro can provide valuable insights into the immune system. This manuscript reviews the critical roles played by different immune cells and surveys the current progress of model systems for reverse engineering of immune microenvironments with a focus on lymphoid tissues.

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Antigen Presenting B Cells Facilitate CD4 T Cell Cooperation Resulting in Enhanced Generation of Effector and Memory CD4 T Cells

Cited by 21 publications

References 40 publications

The Number of Responding CD4 T Cells and the Dose of Antigen Conjointly Determine the Th1/Th2 Phenotype by Modulating B7/CD28 Interactions

The Number of Responding CD4 T Cells and the Dose of Antigen Conjointly Determine the Th1/Th2 Phenotype by Modulating B7/CD28 Interactions

Does T Cell Activation Require a Quorum of Lymphocytes?

Deconstructing Immune Microenvironments of Lymphoid Tissues for Reverse Engineering

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