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Memory B Cells and Pneumococcal Antibody After Splenectomy¹

Heather Wasserstrom^*, James Bussel, Lony C.-L. Lim and Charlotte Cunningham-Rundles^2,*

^* Departments of Medicine, Pediatrics and the Immunology Institute, Mount Sinai Medical Center, New York City, NY 10029; Department of Pediatrics, Weill Medical College, Cornell University, New York City, NY 10021; and Immunology Division, Specialty Laboratories, Valencia, CA 91355

Splenectomized patients are susceptible to bloodstream infections with encapsulated bacteria, potentially due to loss of blood filtering but also defective production of anticarbohydrate Ab. Recent studies propose that a lack of Ab is related to reduced numbers of IgM⁺ CD27⁺ memory B cells found after splenectomy. To test this, we analyzed CD27⁺ memory B cell subsets, IgG, and IgM pneumococcal Ab responses in 26 vaccinated splenectomized subjects in comparison to memory B cell subsets and Ab responses in healthy controls. As shown previously, the splenectomized autoimmune subjects had fewer total, isotype switched, and IgM⁺ CD27⁺ memory B cells as compared with controls, but there was no difference in memory B cells subsets between controls and splenectomized subjects with spherocytosis. There was no difference between the geometric mean IgG Ab response between normal controls and splenectomized subjects (p = 0.51; p = 0.81). Control subjects produced more IgM Ab than splenectomized autoimmune subjects (p = 0.01) but the same levels as subjects with spherocytosis (p = 0.15.) There was no correlation between memory B cell subsets and IgG or IgM Ab responses for controls or splenectomized subjects. These data suggest that splenectomy alone may not be the sole reason for loss of memory B cells and reduced IgM antipneumococcal Ab. Because subjects with autoimmunity had splenectomy at a significantly older age than participants with spherocytosis, these data suggest that an age-related loss of extra splenic sites necessary for the maintenance or function of memory B cells may lead to impaired immunity in these subjects.

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 grants from the National Institutes of Health, AI 101093, AI-467320, AI-48693, the Scientific Advisory Boards of Talecris, Omrix, and Baxter Healthcare, and National Institute of Allergy and Infectious Diseases Contract 03-22 (to C.C.R.) and research support from Amgen, GSK, Cangene, Ligand, Sysmex, Genzyme, Immunomedex, and MGI Pharma (to J.B.B.). H.W. was supported by the Doris Duke Charitable Trust.

² Address correspondence and reprint requests to Dr. Charlotte Cunningham-Rundles, Department of Medicine, Mount Sinai Medical Center, 1425 Madison Avenue, New York City, NY 10029. E-mail address: Charlotte.Cunningham-Rundles{at}MSSM.edu

³ Abbreviations used in this paper: ITP, immune thrombocytopenic purpura; HS, hereditary spherocytosis; AI, autoimmune disease.