Low class switched memory B cells predicts the need for continued need for replacement immunoglobulin therapy post Rituximab use and adequate numeric B cell reconstitution

McNulty, Caitlin M.G.; Joshi, Avni Y.

doi:10.1016/j.jaci.2017.12.267

Cited by 2 publications

(1 citation statement)

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“…Thus, this search for biomarkers of TRS potentially highlights a distinctive immunophenotype of long-term clozapine therapy. Reduced CSMB populations are predictive of immunoglobulin replacement requirement in secondary hypogammaglobulinemia (37). This is in keeping with our initial report 5 (38,39).…”

Section: Immunological Alterations and Possible Pathogenetic Mechanismssupporting

confidence: 89%

Clozapine-associated secondary antibody deficiency

Ponsford

Pecoraro

Jolles

2019

Current Opinion in Allergy &Amp; Clinical Immunology

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Purpose of review: Clozapine has recently been described as a novel cause of secondary antibody deficiency (SAD), associated with long-term therapy. Here we critically review the evidence linking clozapine-use to an increased infection risk, describe immunological alterations, and discuss potential mechanisms. Findings: Individuals with schizophrenia are at 2-5 times more likely to develop pneumonia than the general population, in particular when receiving clozapine. Delayed-onset distinguishes clozapineassociated hypogammaglobulinaemia from agranulocytosis or neutropenia that occur at lesser frequency. Biomarker searches in treatment-resistant schizophrenia highlight an immune signature associated with long-term clozapine use. This includes reduction in class-switched memory B-cells, echoing common variable immunodeficiency. Recent identification of a role for dopamine in T follicular helper-B cell interactions may inform future clinical studies. Summary: The detrimental impact of the increased infection risk associated with clozapine necessitates a re-evaluation of the current monitoring strategies as well as further studies to better understand the underlying mechanisms of SAD in this setting. Based on available evidence, we suggest simple modifications to clozapine monitoring including integration of routine vaccination, smoking cessation, and assessment of humoral immunity. Further studies are required to understand the role of clozapine in neuroinflammation as well as potentially other autoantibody mediated diseases.

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Section: Immunological Alterations and Possible Pathogenetic Mechanismssupporting

confidence: 89%