Basophils Support the Survival of Plasma Cells in Mice

Gómez, Manuel R.; Talke, Yvonne; Goebel, Nicole; Hermann, Fabian; Reich, Barbara; Mack, Matthias

doi:10.4049/jimmunol.1002319

Cited by 119 publications

(84 citation statements)

References 39 publications

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“…However, Mcpt8Cre mice showed decreased frequencies of eosinophils (2.4-fold; P < 0.05) and Th2 cells (twofold; P < 0.05) shortly after reinfection, indicating that basophils induced the early memory type 2 immune response, as previously suggested by others (32). Basophils have been reported to promote the survival of plasma cells in the spleen and to enhance humoral memory responses (33,34). To investigate whether basophil deficiency results in lower antibody levels, we measured serum concentrations of IgE and IgG1 antibodies in Mcpt8Cre and control mice after first and second Hp infection (Fig.…”

Section: Resultssupporting

confidence: 53%

Basophil-mediated protection against gastrointestinal helminths requires IgE-induced cytokine secretion

Schwartz

Turqueti-Neves

Hartmann

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance Gastrointestinal worms (helminths) infect more than 2 billion people, and vaccines are not yet available. Helminths elicit a type 2 immune response characterized by high serum IgE levels and increased numbers of IL-4– or IL-13–secreting effector cells including Th2 cells, eosinophils, basophils, and type 2 innate lymphoid cells. We determined the mechanism by which basophils contribute to protection against secondary infections with gastrointestinal helminths. Here we demonstrate that basophils are recruited into the small intestine of infected mice and orchestrate the local type 2 immune response in this tissue. Basophil-mediated protection required the presence of IgE and the expression of activating Fc receptors and IL-4/IL-13 in basophils. These findings could help the development of new vaccination strategies against helminths.

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Section: Resultssupporting

confidence: 53%

Basophil-mediated protection against gastrointestinal helminths requires IgE-induced cytokine secretion

Schwartz

Turqueti-Neves

Hartmann

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…Our results support the possibility, therefore, that the predisposition to lung infections in TACI-deficient individuals is mediated through a failure to maintain isotype-switched ASCs in the lungs by a mechanism involving CD11b + cells. We are currently investigating CD11b + cell subsets in lungs (Supplemental Figure 8B) as well as lymphoid organs during influenza infection, with particular attention to eosinophils (74) and basophils (75), which have been implicated in controlling ASC survival.…”

Section: Discussionmentioning

confidence: 99%

Protective antiviral antibody responses in a mouse model of influenza virus infection require TACI

Wolf¹,

Mozdzanowska²,

Quinn³

et al. 2011

J. Clin. Invest.

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Antiviral Abs, for example those produced in response to influenza virus infection, are critical for virus neutralization and defense against secondary infection. While the half-life of Abs is short, Ab titers can last a lifetime due to a subset of the Ab-secreting cells (ASCs) that is long lived. However, the mechanisms governing ASC longevity are poorly understood. Here, we have identified a critical role for extrinsic cytokine signals in the survival of respiratory tract ASCs in a mouse model of influenza infection. Irradiation of mice at various time points after influenza virus infection markedly diminished numbers of lung ASCs, suggesting that they are short-lived and require extrinsic factors in order to persist. Neutralization of the TNF superfamily cytokines B lymphocyte stimulator (BLyS; also known as BAFF) and a proliferation-inducing ligand (APRIL) reduced numbers of antiviral ASCs in the lungs and bone marrow, whereas ASCs in the spleen and lung-draining lymph node were surprisingly unaffected. Mice deficient in transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), a receptor for BLyS and APRIL, mounted an initial antiviral B cell response similar to that generated in WT mice but failed to sustain protective Ab titers in the airways and serum, leading to increased susceptibility to secondary viral challenge. These studies highlight the importance of TACI signaling for the maintenance of ASCs and protection against influenza virus infection.

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“…Stromal cells, eosinophils, and megakaryocytes secreting CXCL12, IL-6, and APRIL have been shown to interact with long-lived PC in bone marrow, and IL-6-secreting basophils and stromal cells have been shown to interact with PC in the spleen (27,(36)(37)(38)(39)(40)(41). A specific inflammatory milieu could promote the residence of long-lived PC in rituximab-treated patients, since RTX-PC survived better than control ones upon in vitro incubation of total splenic cells.…”

Section: Discussionmentioning

confidence: 99%

B cell depletion in immune thrombocytopenia reveals splenic long-lived plasma cells

Mahévas¹,

Patin²,

Huetz³

et al. 2012

J. Clin. Invest.

165

151

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Primary immune thrombocytopenia (ITP) is a disorder caused by autoantibody-mediated platelet destruction and decreased platelet production. Rituximab, a B cell-depleting agent, has become the first-line treatment for ITP; however, patients with refractory disease usually require splenectomy. We identified antibody-secreting cells as the major splenic B cell population that is resistant to rituximab. The phenotype, antibody specificity, and gene expression profile of these cells were characterized and compared to those of antibody-secreting cells from untreated ITP spleens and from healthy tissues. Antiplatelet-specific plasma cells (PC) were detected in the spleens of patients with ITP up to 6 months after rituximab treatment, and the PC population displayed a long-lived program similar to the one of bone marrow PC, thus explaining for most of these patients the absence of response to rituximab and the response to splenectomy. When analyzed by multiplex PCR at the single-cell level, normal splenic PC showed a markedly different gene expression profile, with an intermediate signature, including genes characteristic of both long-lived PC and proliferating plasmablasts. Surprisingly, long-lived PC were not detected in untreated ITP spleens. These results suggest that the milieu generated by B cell depletion promotes the differentiation and settlement of long-lived PC in the spleen.

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Basophils Support the Survival of Plasma Cells in Mice

Cited by 119 publications

References 39 publications

Basophil-mediated protection against gastrointestinal helminths requires IgE-induced cytokine secretion

Basophil-mediated protection against gastrointestinal helminths requires IgE-induced cytokine secretion

Protective antiviral antibody responses in a mouse model of influenza virus infection require TACI

B cell depletion in immune thrombocytopenia reveals splenic long-lived plasma cells

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