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Loss of Discrete Memory B Cell Subsets Is Associated with Impaired Immunization Responses in HIV-1 Infection and May Be a Risk Factor for Invasive Pneumococcal Disease¹

Melanie Hart^*, Alan Steel^*, Sally A. Clark^*, Graeme Moyle, Mark Nelson, Don C. Henderson, Robert Wilson, Frances Gotch^*, Brian Gazzard and Peter Kelleher^2,*

^* Department of Immunology, Imperial College, Chelsea and Westminster Hospital, London, United Kingdom; HIV/GUM Directorate, Chelsea and Westminster Foundation, National Health Service (NHS) Trust, London, United Kingdom; Division of Immunology, Hammersmith Hospitals, NHS Trust, London, United Kingdom; and Department of Respiratory Medicine, Royal Brompton and Harefield, NHS Trust, London, United Kingdom

Invasive pneumococcal infection is an important cause of morbidity and mortality in HIV-1-infected individuals. B cells play an important role in maintaining serologic memory after infection. IgM memory B cells are significantly reduced in HIV-1-infected patients and their frequency is similar to that observed in other patient groups (splenectomized individuals and patients with primary Ab deficiency) who are also known to have an increased risk of invasive pneumococcal infection. Antiretroviral therapy does not restore marginal zone B cell percentages. Immunization with the 23-valent polysaccharide pneumococcal vaccine shows that HIV-1-infected patients have impaired total IgM and IgG pneumococcal vaccines compared with healthy controls. Loss of switched memory B cells was associated with impaired tetanus toxoid IgG vaccine responses. Results of this study demonstrate that defects in B cell memory subsets are associated with impaired humoral immune responses in HIV-1 patients who are receiving antiretroviral therapy and may be a contributory factor to the increased risk of invasive pneumococcal infection observed in HIV-1 infection.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by the St. Stephens AIDS Trust (to S.A.C., A.S., and P.K.), the Luard Foundation (to A.S.), the Joint Research Committee of Chelsea and Westminster National Health Service Trust (to M.H. and P.K.), and Abbott Laboratories (to A.S.).

² Address correspondence and reprint requests to Dr. Peter Kelleher, Department of Immunology, Imperial College, Chelsea and Westminster Hospital, London SW10 9NH, U.K. E-mail address: p.kelleher{at}imperial.ac.uk

³ Abbreviations used in this paper: ART, antiretroviral therapy; HC, healthy control; CVID, common variable immune deficiency; BAFF, B cell-activating factor; APRIL, a proliferating-inducing ligand; MBO, memory B cell O; MZB, marginal zone B cell.