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DOI 10.1128/iai.05094-11

Медицинская библиотека · Infection and immunity · 2011

CD23b isoform expression in human schistosomiasis identifies a novel subset of activated B cells.

Onguru Daniel, Liang YanMei, Elliot Jennifer, Mwinzi Pauline, Ganley-Leal Lisa

СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

Resistance to schistosomiasis is associated with increased levels of serum parasite-specific IgE. IgE exerts its functions through its cellular receptors, FcεRI and FcεRII/CD23; however, its functional significance in humans requires further characterization. We previously reported that increased levels of CD23(+) B cells correlate with resistance to schistosomiasis in hyperexposed populations and sought to define their potential function and relationship with IgE. We found that CD23(+) B cells are a heterogeneous cell population with functional and phenotypic differences. Circulating CD23(+) B cells are uniquely activated in schistosomiasis and express the CD23b isoform and CXCR5, the homing receptor for lymphoid follicles. High CXCR5 expression by CD23(+) B cells was associated with the capacity to home to the cognate ligand CXCL13. CD23-bound IgE cross-linking increased surface expression of CXCR5, suggesting that CD23(+) B cells home directly into the lymphoid follicles upon antigen capture. As human schistosomiasis is an intravascular parasitic infection associated with a high antigenic burden in the blood, circulating CD23(+) B cells may play a role in the capture and shuttling of antigens directly to splenic follicles, highlighting a new role for circulating B cells. This function likely plays an important role in the development of protective immunity to infection with schistosomes.

Для цитирования: Onguru Daniel, Liang YanMei, Elliot Jennifer, Mwinzi Pauline, Ganley-Leal Lisa. CD23b isoform expression in human schistosomiasis identifies a novel subset of activated B cells.. Infection and immunity. 2011. DOI: 10.1128/iai.05094-11.

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