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B cells join T cell clusters in the host response to recurrent herpes simplex virus 2 infection
Jeff R. Gehlhausen, Akiko Iwasaki
Jeff R. Gehlhausen, Akiko Iwasaki
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B cells join T cell clusters in the host response to recurrent herpes simplex virus 2 infection

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Abstract

Recurrent genital herpes lesions are infiltrated by various leukocytes, yet the role of B cell subsets in this process is unknown. In this issue of the JCI, Ford et al. describe the presence and antibody-secreting role of local B cell populations in herpes simplex virus 2 (HSV-2) recurrent lesions. The authors analyzed a comprehensive array of sequential skin biopsy specimens from HSV-2–infected patients over time and at various stages of infection. Using immunofluorescence and in situ hybridization, the authors show the presence of rare IgD+ naive B cells and IgG-expressing antibody-secreting cells (ASCs) in recurrent HSV-2 lesions embedded in CD4+ T cell–rich dermal immune infiltrates, levels of which transiently increase during lesion reactivation and healing. Notably, local increases in HSV-2–specific antibodies in recurrent lesions were detected, whereas serum HSV-2 antibody levels remained stable. Future research is needed to understand the precise role of these tissue-visiting B cells in disease resolution.

Authors

Jeff R. Gehlhausen, Akiko Iwasaki

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