Regulatory Roles for Cytokine- Producing B Cells in Infection and Autoimmune Disease

Lund, Frances E.; Garvy, Beth A.; Randall, Troy D.; Harris, David P.

doi:10.1159/000082086

Cited by 162 publications

(131 citation statements)

References 135 publications

(180 reference statements)

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“…Rather, we show that B cells regulate the emergence of Treg cells in the CNS in a B7-dependent manner. It is becoming increasingly clear that B cells can regulate immune responses in a variety of ways; thus in their absence T cell defects may vary depending on the experimental condition (32,33).…”

Section: Discussionmentioning

confidence: 99%

B Cell Regulation of CD4+CD25+ T Regulatory Cells and IL-10 Via B7 is Essential for Recovery From Experimental Autoimmune Encephalomyelitis

Mann

Maresz

Shriver

et al. 2007

The Journal of Immunology

276

219

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CD4+CD25+ T regulatory (Treg) cells expressing the Foxp3 transcription factor have been shown to be present in the CNS during the autoimmune disease experimental autoimmune encephalomyelitis (EAE) and can inhibit EAE clinical disease by an IL-10-dependent mechanism. In addition, IL-10 expression in the CNS late in the EAE disease course has been attributed to recovery. However, it is not known how Treg cells and IL-10 expressions are regulated during EAE. We have previously shown a requirement for B cells in recovery from EAE and here investigated whether this was due to a deficiency in Treg cells and IL-10 in the CNS. We found that B cell deficiency resulted in a delay in the emergence of Foxp3-expressing Treg cells and IL-10 in the CNS during EAE, but not in the periphery. Reconstitution with wild-type B cells resulted in disease recovery and normalized IL-10 and Foxp3 expression. However, reconstitution with B7-deficient B cells did not. Furthermore, we show that IL-10 and Foxp3 expression is enhanced in CNS nonencephalitogenic T cells. These data suggest a novel mechanism whereby B cells regulate CD4+CD25+ Treg cells via B7 and subsequently enter the CNS and suppress autoimmune inflammation, mediating recovery.

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Section: Discussionmentioning

confidence: 99%

B Cell Regulation of CD4+CD25+ T Regulatory Cells and IL-10 Via B7 is Essential for Recovery From Experimental Autoimmune Encephalomyelitis

Mann

Maresz

Shriver

et al. 2007

The Journal of Immunology

276

219

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“…They are both effective antigen-presenting cells and activators of T cells (33) and also produce proinflammatory cytokines and chemokines (34)(35)(36). Indeed, rituximab treatment in rheumatoid arthritis has been shown to lead to depletion of other major cell populations, such as T cells and macrophages within synovial tissue (37).…”

Section: Discussionmentioning

confidence: 99%

Rituximab is effective in the treatment of refractory ophthalmic Wegener's granulomatosis

Taylor¹,

Salama²,

Joshi³

et al. 2009

Arthritis & Rheumatism

170

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Objective. To investigate the efficacy of rituximab in patients with refractory ophthalmic Wegener's granulomatosis (WG).Methods. Data from 10 consecutive patients with refractory ophthalmic WG treated with rituximab were retrospectively reviewed. In all patients, the ophthalmic disease was driving treatment decisions, and disease activity had persisted despite standard immunosuppressive treatment. Patients had refractory scleritis (n ‫؍‬ 3), orbital granulomas causing optic nerve compromise (n ‫؍‬ 4), or a combination of both conditions (n ‫؍‬ 3). All patients had been treated with at least 3 different immunosuppressive agents, and 5 patients had previously been treated with tumor necrosis factor ␣ blockade. Rituximab was administered intravenously in 2 doses, 2 weeks apart, in combination with standard treatment. Disease activity was monitored clinically by an interdisciplinary approach, including disease activity scoring, immunodiagnostics, and magnetic resonance imaging, as well as by corresponding reductions in the required dose of conventional medication.

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“…The fact that both surface and intracellular TCR levels are down-regulated in sOVA Tg TCR␣ Ϫ/Ϫ recipients suggests that both internalization and degradation occur. B cells may also inhibit T cell differentiation by producing inhibitory cytokines such as IL-10 and TGF␤ (25,26).…”

Section: Tcr Down-modulation On Self-ag-specific T Cells In the Presementioning

confidence: 99%

Cutting Edge: The Link between Lymphocyte Deficiency and Autoimmunity: Roles of Endogenous T and B Lymphocytes in Tolerance

Knoechel

Lohr

Kahn

et al. 2005

The Journal of Immunology

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We demonstrate that transfer of OVA-specific DO11 CD4+ T cells into mice that lack T and B cells and produce secreted OVA as an endogenous self-protein results in a severe systemic autoimmune reaction with skin inflammation, wasting, and death. The transferred DO11 T cells undergo massive expansion and produce IL-2 and IFN-γ abundantly. Transfer of DO11 cells into OVA-expressing animals in which T cells are absent but B cells are present, leads to mild disease with no death. In this situation, the DO11 cells undergo similar expansion but show poor Th1 differentiation. This regulatory effect of B cells correlates with profound TCR down-regulation. If T cells are present, the DO11 cells fail to expand independent of B cells. These results suggest that both endogenous T and B lymphocytes control T cell tolerance induction and pathogenicity, but at different stages of an anti-self response. Although endogenous T cells prevent expansion and maintain homeostasis, endogenous B cells limit subsequent effector responses of autoreactive CD4+ T cells.

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Regulatory Roles for Cytokine- Producing B Cells in Infection and Autoimmune Disease

Cited by 162 publications

References 135 publications

B Cell Regulation of CD4+CD25+ T Regulatory Cells and IL-10 Via B7 is Essential for Recovery From Experimental Autoimmune Encephalomyelitis

B Cell Regulation of CD4+CD25+ T Regulatory Cells and IL-10 Via B7 is Essential for Recovery From Experimental Autoimmune Encephalomyelitis

Rituximab is effective in the treatment of refractory ophthalmic Wegener's granulomatosis

Cutting Edge: The Link between Lymphocyte Deficiency and Autoimmunity: Roles of Endogenous T and B Lymphocytes in Tolerance

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