Immune Response After Splenectomy

Sullivan, JohnL.; Schiffman, Gerald; Miser, James S.; Ochs, HansD.; Hammerschlag, M R; Vichinsky, E.; Wedgwood, RalphJ.

doi:10.1016/s0140-6736(78)90612-8

Cited by 219 publications

(66 citation statements)

References 9 publications

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“…Quantitative immunoglobulins were determined by standard radial immunodiffusion or nephelometric techniques. Pneumococcal capsular polysaccharide antibodies were determined by a sensitive radioimmunoassay (16). Viral antibodies (excluding EBV) were determined at the Massachusetts State Laboratory, Jamaica Plain, MA. Antibody titers to EBV-VCA, EA, and EBNA were determined by established methods (17,18).…”

Section: Cytotoxicity Studiesmentioning

confidence: 99%

X-linked lymphoproliferative syndrome. Natural history of the immunodeficiency.

Sullivan¹,

Byron²,

Brewster³

et al. 1983

J. Clin. Invest.

120

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A B S T R A C T The X-linked lymphoproliferative syndrome is characterized by immunodeficiency to Epstein-Barr virus (EBV) manifested by severe or fatal infectious mononucleosis and acquired immunodeficiency. We studied immune responses in six males of a well-characterized kindred with the X-linked lymphoproliferative syndrome. Two males were studied before and during acute fatal EBV infection. Both individuals demonstrated normal cellular and humoral immunity before EBV infection. During acute EBV infection, both individuals developed vigorous cytotoxic cellular responses against EBV-infected and -iipinfected target cells. Anomalous killer and natural killer T cell activity was demonstrated against a va'-riety of lymphoid cell lines, autologous fibroblasts and autologous hepatocytes. Effector cells responsible for anomalous killing reacted with a pan-T cell monoclonal antibody, and belonged to the OKT.8 T cell subset. Death in each case was caused by liver failure, but one patient developed extensive liver necrosis, whereas the other developed a massive infiltration of the liver with EBV-infected immunoblasts after aggressive immunosuppressive therapy. Immunological studies were performed on four males who had survived EBV infection years previously. They demonstrated global cellular immune defects with deficiencies of lymphocyte proliferative responses to mitogens and antigens, humoral immune deficiencies, abnormalities of regulatory T cell subsets and deficient natural killer cell activity. We propose that an aberrant immune response triggered by acute EBV infection results in unregulated anomalous killer and natural killer cell activity against EBV infected and uninfected cells. These studies suggest that global immune defects appearing in males with X-linked lymphopro-

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Section: Cytotoxicity Studiesmentioning

confidence: 99%

X-linked lymphoproliferative syndrome. Natural history of the immunodeficiency.

Sullivan¹,

Byron²,

Brewster³

et al. 1983

J. Clin. Invest.

120

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“…The immunogenicity of PPS vaccine in splenectomized patients has been assessed in a number of trials. Some studies have shown the effectiveness of vaccination in inducing protective concentrations of specific antibodies (5,10,24,33), while others have shown limited serological responses (15). As the initiation of the antibody response to polysaccharides seems to depend on the presence of splenic tissue, and in particular on a functional marginal-zone B-cell compartment (3,14,18,34), it may be expected that polysaccharide vaccines are of limited use in asplenic patients.…”

mentioning

confidence: 99%

Pneumococcal Conjugate Vaccines Overcome Splenic Dependency of Antibody Response to Pneumococcal Polysaccharides

Breukels

Zandvoort²,

Dobbelsteen

et al. 2001

Infect Immun

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Protection against infections with Streptococcus pneumoniae depends on the presence of antibodies against capsular polysaccharides that facilitate phagocytosis. Asplenic patients are at increased risk for pneumococcal infections, since both phagocytosis and the initiation of the antibody response to polysaccharides take place in the spleen. Therefore, vaccination with pneumococcal polysaccharide vaccines is recommended prior to splenectomy, which, as in the case of trauma, is not always feasible. We show that in rats, vaccination with a pneumococcal conjugate vaccine can induce good antibody responses even after splenectomy, particularly after a second dose. The spleen remains necessary for a fast, primary response to (blood-borne) polysaccharides, even when they are presented in a conjugated form. Coadministration of a conjugate vaccine with additional nonconjugated polysaccharides of other serotypes did not improve the response to the nonconjugated polysaccharides. We conclude that pneumococcal conjugate vaccines can be of value in protecting asplenic or hyposplenic patients against pneumococcal infections.Protection against infections with encapsulated bacteria such as Streptococcus pneumoniae depends on the presence of antibodies against capsular polysaccharides. These serotypespecific antibodies facilitate phagocytosis, the main mode of host defense against S. pneumoniae. The spleen is an important organ in the immune response to S. pneumoniae, since it contains both antibody-producing B cells and phagocytes (4, 26). Asplenic patients are therefore at increased risk for invasive infections with S. pneumoniae (13). Although most infections occur within the first few years after splenectomy, the risk of overwhelming postsplenectomy infections is lifelong (9, 36). Therefore, vaccination against S. pneumoniae is indicated for this group. At present, the vaccine available for this aim is the 23-valent pneumococcal polysaccharide (PPS) vaccine (1). The immunogenicity of PPS vaccine in splenectomized patients has been assessed in a number of trials. Some studies have shown the effectiveness of vaccination in inducing protective concentrations of specific antibodies (5, 10, 24, 33), while others have shown limited serological responses (15). As the initiation of the antibody response to polysaccharides seems to depend on the presence of splenic tissue, and in particular on a functional marginal-zone B-cell compartment (3,14,18,34), it may be expected that polysaccharide vaccines are of limited use in asplenic patients.The physical coupling of a polysaccharide to a carrier protein greatly improves the immunogenicity of the polysaccharide, a principle first described in 1929 (11). Conjugated polysaccharides overcome the antipolysaccharide unresponsiveness in early life (2, 8), which is thought to be due to a still immature splenic marginal-zone B-cell compartment (2). The induction of antipolysaccharide antibodies by conjugate vaccines at a young age suggests that conjugates might initiate the antipolysaccharide anti...

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“…1972). The primary antibody response to an intravenously administered antigen is decreased or absent, and the secondary response is also abnormal, including a defect in the normal switching from IgM to IgG (Lozzio and Wargon, 1974;Baker et al, 1975;Sullivan et al, 1978). However, the response to antigen presented orally, intradermally, intraperitoneally or intramuscularly is normal (Rowley, 1950).…”

Section: Discussionmentioning

confidence: 99%

THE EFFECT OF SPLENECTOMY ON THE PRODUCTION OF ABLASTIN AND THE TERMINATION OF THE PARASITAEMIA IN RATS INFECTED WITH TRYPANOSOMA LEWISI

Drew¹,

Jenkin

1983

Aust J Exp Biol Med

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Summary. This study investigated the effect of splenectomy on the production of ablastin and the elimination of Trypanosoma lc\vi.s-i from the circulation of infected Porton rats. Rats were .splenectomized or sham-splenectomized either before or at various stages during the infection and ihe course of the parasitaemia compared with untreated control animals. Ablastin titres in the serum were measured by a sensitive in vitro assay and were found to be the same in all the rats, regardless of the nature or timing of the operation. Splenectomized animals eliminated the parasite more slowly from the circulation than either the shamsplenectomized animals or unoperated controls. It is concluded that the presence of the spleen enables the rat to clear the parasite more rapidly from the circulation, but that the spteen h not essential for the production ablastin during the infection.

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Immune Response After Splenectomy

Cited by 219 publications

References 9 publications

X-linked lymphoproliferative syndrome. Natural history of the immunodeficiency.

X-linked lymphoproliferative syndrome. Natural history of the immunodeficiency.

Pneumococcal Conjugate Vaccines Overcome Splenic Dependency of Antibody Response to Pneumococcal Polysaccharides

THE EFFECT OF SPLENECTOMY ON THE PRODUCTION OF ABLASTIN AND THE TERMINATION OF THE PARASITAEMIA IN RATS INFECTED WITH TRYPANOSOMA LEWISI

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