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Long-lived Plasma Cells (long-lived + plasma_cell)
Selected AbstractsIntranasal immunisation with inactivated RSV and bacterial adjuvants induces mucosal protection and abrogates eosinophilia upon challengeEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 5 2006Nathalie Etchart Abstract We have previously shown that following intranasal exposure to influenza virus, specific plasma cells are generated in the nasal-associated lymphoid tissue (NALT) and maintained for the life of the animal. However, we also showed that following infection with respiratory syncytial virus (RSV), specific plasma cells are generated in the NALT but wane quickly and are not maintained even after challenge, even though RSV-specific serum antibody responses remain robust. Only infection with influenza virus generated sterilising immunity, implying a role for these long-lived plasma cells in protection. We show here that the RSV-specific IgA NALT plasma cell population and lung antibody levels can be substantially boosted, both at acute and memory time points, by intranasal immunisation with inactivated RSV (iRSV) in combination with bacterial outer membrane vesicles (OMV) compared to live RSV alone. Finally, challenge with live RSV showed that immunisation with iRSV and OMV protect against both virus replication in the lung and the eosinophil infiltrate generated by either live RSV or iRSV alone. These data show that immunisation with iRSV and OMV maintains a NALT RSV-specific plasma cell population and generates an efficient protective immune response following RSV infection. See accompanying commentary: http://dx.doi.org/10.1002/eji.200636118 [source] Transcription factors that regulate memory in humoral responsesIMMUNOLOGICAL REVIEWS, Issue 1 2006Kathryn Calame Summary:, At least three types of B lymphocytes are important for providing memory in a humoral immune response: ,classical' memory cells that do not secrete immunoglobulin (Ig), long-lived plasma cells (LLPCs) in the bone marrow, and ,innate-like' B-1 cells. In this review, our work on B-lymphocyte-induced maturation protein-1 (Blimp-1), a critical regulator of terminal B-cell differentiation, is discussed in the context of current knowledge of all transcriptional controls that regulate these three types of B cells. Blimp-1 is not required for formation of memory cells, but it is required for them to progress toward becoming plasma cells. Blimp-1 is required for Ig secretion in plasma cells and in B-1 cells. Induction of the activator X-box-binding protein-1 and formation of µ-secreted mRNA depend on Blimp-1 in both cell types. Finally, even after their formation, LLPCs in the bone marrow continue to require Blimp-1 for their maintenance. [source] Bortezomib as the Sole Post-Renal Transplantation Desensitization Agent Does Not Decrease Donor-Specific Anti-HLA AntibodiesAMERICAN JOURNAL OF TRANSPLANTATION, Issue 3 2010R. Sberro-Soussan Persistence of donor-specific anti-HLA antibodies (DSA) associated with antibody-mediated graft injuries following kidney transplantation predicts evolution toward chronic humoral rejection and reduced graft survival. Targeting plasma cells, the main antibody-producing cells, with the proteasome inhibitor bortezomib may be a promising desensitization strategy. We evaluated the in vivo efficacy of one cycle of bortezomib (1.3 mg/m2× 4 doses), used as the sole desensitization therapy, in four renal transplant recipients experiencing subacute antibody-mediated rejection with persisting DSA (>2000 [Mean Fluorescence Intensity] MFI). Bortezomib treatment did not significantly decrease DSA MFI within the 150-day posttreatment period in any patient. In addition, antivirus (HBV, VZV and HSV) antibody levels remained stable following treatment suggesting a lack of efficacy on long-lived plasma cells. In conclusion, one cycle of bortezomib alone does not decrease DSA levels in sensitized kidney transplant recipients in the time period studied. These results underscore the need to evaluate this new desensitization agent properly in prospective, randomized and well-controlled studies. [source] Viral load determines the B-cell response in the cerebrospinal fluid during human immunodeficiency virus infectionANNALS OF NEUROLOGY, Issue 5 2007Sabine Cepok PhD Objective Human immunodeficiency virus (HIV) infection of the central nervous system (CNS) is frequently associated with intrathecal immunoglobulin synthesis and cerebrospinal fluid (CSF) pleocytosis, but little is known about the B-cell response in the CSF of these patients. In this study, we investigated the relation between virus load and the frequency and phenotype of B cells in the CSF of HIV-infected patients. Methods The distribution of T cells, B cells, short-lived plasmablasts, and long-lived plasma cells was analyzed by flow cytometry in CSF and peripheral blood of 33 patients with HIV infection compared with 12 patients with noninfectious CNS diseases. HIV RNA copy number in CSF and serum was quantified by kinetic polymerase chain reaction. Results B-cell and plasmablast levels were increased in the CSF of HIV-infected patients compared with patients with noninfectious CNS diseases. Whereas CSF B cells were found at similar frequency during early and late stages of HIV infection, plasmablasts were more prevalent in the CSF during early infection. Plasmablasts in the CSF correlated with intrathecal IgG synthesis and even stronger with HIV RNA copy numbers in CSF, in particular, in untreated, early HIV-infected individuals. Initiation of antiviral treatment in therapy-naive patients strongly decreased HIV copy numbers and plasmablasts in CSF. Interpretation Our findings demonstrate that HIV infection of the CNS triggers an early profound B-cell response, with plasmablasts serving as the main virus-related B-cell subset in the CSF. Ann Neurol 2007 [source] Limited humoral immunoglobulin E memory influences serum immunoglobulin E levels in bloodCLINICAL & EXPERIMENTAL ALLERGY, Issue 9 2009G. Achatz-Straussberger Summary The switch of B cells expressing membrane-bound Igs, which serve as antigen receptors, to antibody-secreting plasmablasts and finally to non-dividing, long-lived plasma cells (PCs) lacking an antigen receptor, marks the terminal differentiation of a B cell. Antibody-secreting PCs represent the key cell type for the maintenance of a proactive humoral immunological memory. Although some populations of long-lived PCs persist in the spleen, most of them return to their ,place of birth' and travel to the bone marrow or invade inflamed tissues, where they survive up to several months in survival niches as resident, immobile cells. Existing data strongly support the notion that isotype-specific receptor signalling influences the migration behaviour of plasmablasts to the bone marrow. The recent observation in the murine sytem that the immigration of plasmablasts and the final differentiation to long-lived PCs in the bone marrow is dependent on the expressed B-cell isotype and the related expression of chemokine receptors leads to the conclusion that during a T-helper type 2 (Th2)-mediated immune response in wild type mice, IgE plasmablasts do not have the same chance to contribute to long-lived PC memory as IgG1 plasmablasts. The overall limited humoral IgE memory additionally restricts the quantity of IgE Igs in the serum. [source] | ||||||||||