The Deadly Dance of B Cells with Trypanosomatids. Issue 2 (February 2018)

• Record Type: Journal Article
• Authors: Silva-Barrios, Sasha; Charpentier, Tania; Stäger, Simona
• Is Part Of: Trends in parasitology. Volume 34:Issue 2(2018)
• Page Start: 155
• Page End: 171
• Publication Date: 2018-02
• Subjects: B cells -- tripanosomatids -- hypergammaglobulinemia -- polyclonal B cell activation; Parasitology -- Periodicals; Parasitology -- Periodicals; Biology -- Periodicals; Parasitology; Biology; Parasitologie -- Périodiques; Online resources; 571.999
• DOI: 10.1016/j.pt.2017.10.001
• Languages: English
• ISSNs: 1471-4922

Abstract

Abstract : B cells are notorious actors for the host's protection against several infectious diseases. So much so that early vaccinology seated its principles upon their long-term protective antibody secretion capabilities. Indeed, there are many examples of acute infectious diseases that are combated by functional humoral responses. However, some chronic infectious diseases actively induce immune deregulations that often lead to defective, if not deleterious, humoral immune responses. In this review we summarize how Leishmania and Trypanosoma spp. directly manipulate B cell responses to induce polyclonal B cell activation, hypergammaglobulinemia, low-specificity antibodies, limited B cell survival, and regulatory B cells, contributing therefore to immunopathology and the establishment of persistent infections. Trends: B cells are overactivated during infection with trypanosomatids. This overactivation has a negative impact on disease outcome. In the case of Leishmania, B cell activation results in the generation of immunosuppressive B cells that inhibit protective Th1 responses and induce detrimental Th2 cells. Leishmania donovani activates B cells by triggering endosomal Toll-like receptors and inducing type I interferons (IFN-I). This activation is amplified by IFN-I and ultimately results in an uncontrolled production of low-affinity antibodies. Trypanosoma cruzi metabolic products can directly activate B cells. Besides subverting B cell functions by overactivating them, Trypanosoma brucei also induces an irreversible depletion of some B cell subpopulations in the spleen and hinders B cell maturation and differentiation in the bone marrow.