A Model B-Cell Superantigen and the Immunobiology of B Lymphocytes

Silverman, Gregg J.; Goodyear, Carl S.

doi:10.1006/clim.2001.5143

Cited by 65 publications

(64 citation statements)

References 86 publications

(52 reference statements)

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“…Viral superantigens interacting with T or B cells could potentially cause the lymphoid hyperactivation we observed (43,44), but PRRSV has not been shown to express any T or B cell superantigens. Furthermore, activation by most T and B cell superantigens is characterized by clonal anergy or a short burst of clonal proliferation followed by deletion.…”

Section: Discussionmentioning

confidence: 87%

“…However, staphylococcal protein A targets the framework region of all B cell receptors encoded by the V H 3 family in mice, humans, and swine (Ref. 44; G. J. Silverman, unpublished observations), and all porcine B cell receptors are encoded by V H 3 (45). Thus a direct viral-B cell interaction resulting in B cell hyperplasia cannot be ruled out.…”

Section: Discussionmentioning

confidence: 99%

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Lymphoid Hyperplasia Resulting in Immune Dysregulation Is Caused by Porcine Reproductive and Respiratory Syndrome Virus Infection in Neonatal Pigs

Lemke¹,

Haynes

Spaete

et al. 2004

The Journal of Immunology

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Amid growing evidence that numerous viral infections can produce immunopathology, including nonspecific polyclonal lymphocyte activation, the need to test the direct impact of an infecting virus on the immune system of the host is crucial. This can best be tested in the isolator piglet model in which maternal and other extrinsic influences can be excluded. Therefore, neonatal isolator piglets were colonized with a benign Escherichia coli, or kept germfree, and then inoculated with wild-type porcine reproductive and respiratory syndrome virus (PRRSV) or sham medium. Two weeks after inoculation, serum IgM, IgG, and IgA levels were 30- to 50-, 20- to 80-, and 10- to 20-fold higher, respectively, in animals receiving virus vs sham controls, although <1% was virus specific. PRRSV-infected piglets also had bronchial tree-associated lymph nodes and submandibular lymph nodes that were 5–10 times larger than colonized, sham-inoculated animals. Size-exclusion fast performance liquid chromatography revealed that PRRSV-infected sera contained high-molecular-mass fractions that contained IgG, suggesting the presence of immune complexes. Lesions, inflammatory cell infiltration, glomerular deposits of IgG, IgM, and IgA, and Abs of all three isotypes to basement membrane and vascular endothelium were observed in the kidneys of PRRSV-infected piglets. Furthermore, autoantibodies specific for Golgi Ags and dsDNA could be detected 3–4 wk after viral inoculation. These data demonstrate that PRRSV induces B cell hyperplasia in isolator piglets that leads to immunologic injury and suggests that the isolator piglet model could serve as a useful model to determine the mechanisms of virus-induced immunopathology in this species.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Lymphoid Hyperplasia Resulting in Immune Dysregulation Is Caused by Porcine Reproductive and Respiratory Syndrome Virus Infection in Neonatal Pigs

Lemke¹,

Haynes

Spaete

et al. 2004

The Journal of Immunology

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“…Another mechanism by which GALT could develop is through Ag-independent stimulation of B cells by a molecule, such as a B cell superantigen. To test whether a B cell superantigen could induce GALT development in the GF-Apx rabbits, we introduced a model B cell superantigen, protein A of Staphylococcus aureus (31), into the lumen of the GF-Apx. Whereas the introduction of recombinant protein A alone did not induce GALT development ( Fig.…”

Section: B Cell Superantigen and Galt Developmentmentioning

confidence: 99%

“…Bacteria might promote GALT development by stimulating B cells in a polyclonal manner, via a B cell superantigen, similar to protein A of Staphylococcus aureus (31) and protein L of Peptostreptococcus magnus (45). In this scenerio, a B. subtilis molecule(s) could interact with the B cell receptor of all B cells at a site other than the Ag binding site, thereby directly stimulating proliferation.…”

Section: B Cell Stimulation In Galtmentioning

confidence: 99%

Role of Commensal Bacteria in Development of Gut-Associated Lymphoid Tissues and Preimmune Antibody Repertoire

Rhee

Sethupathi

Driks

et al. 2004

The Journal of Immunology

329

263

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Intestinal bacteria are required for development of gut-associated lymphoid tissues (GALT), which mediate a variety of host immune functions, such as mucosal immunity and oral tolerance. In rabbits, the intestinal microflora are also required for developing the preimmune Ab repertoire by promoting somatic diversification of Ig genes in B cells that have migrated to GALT. We studied the mechanism of bacteria-induced GALT development. Bacteria were introduced into rabbits in which the appendix had been rendered germfree by microsurgery (we refer to these rabbits as germfree-appendix rabbits). We then identified specific members of the intestinal flora that promote GALT development. The combination of Bacteroides fragilis and Bacillus subtilis consistently promoted GALT development and led to development of the preimmune Ab repertoire, as shown by an increase in somatic diversification of VDJ-Cμ genes in appendix B cells. Neither species alone consistently induced GALT development, nor did Clostridium subterminale, Escherichia coli, or Staphylococcus epidermidis. B. fragilis, which by itself is immunogenic, did not promote GALT development; hence, GALT development in rabbits does not appear to be the result of an Ag-specific immune response. To identify bacterial pathways required for GALT development, we introduced B. fragilis along with stress-response mutants of B. subtilis into germfree-appendix rabbits. We identified two Spo0A-controlled stress responses, sporulation and secretion of the protein YqxM, which are required for GALT development. We conclude that specific members of the commensal, intestinal flora drive GALT development through a specific subset of stress responses.

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“…Normal human peripheral blood B lymphocytes can be expanded in vitro through a variety of different stimuli [1][2][3][4][5][6]. However, using a combination of CD40 stimulation in the presence of interleukin (IL)-2, IL-4 and IL-10 appears to be a good stimulus for expansion of human and other animal B lymphocytes in vitro [7][8][9][10], and also plays a significant role in the normal development and function of B lymphocytes [11][12][13][14] as well as in the propagation of malignant B lymphocytes [15].…”

Section: Introductionmentioning

confidence: 99%

c-Src tyrosine kinase co-associates with and phosphorylates signal transducer and activator of transcription 5b which mediates the proliferation of normal human B lymphocytes

Cayer

Proulx

et al. 2009

Clinical and Experimental Immunology

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A Model B-Cell Superantigen and the Immunobiology of B Lymphocytes

Cited by 65 publications

References 86 publications

Lymphoid Hyperplasia Resulting in Immune Dysregulation Is Caused by Porcine Reproductive and Respiratory Syndrome Virus Infection in Neonatal Pigs

Lymphoid Hyperplasia Resulting in Immune Dysregulation Is Caused by Porcine Reproductive and Respiratory Syndrome Virus Infection in Neonatal Pigs

Role of Commensal Bacteria in Development of Gut-Associated Lymphoid Tissues and Preimmune Antibody Repertoire

c-Src tyrosine kinase co-associates with and phosphorylates signal transducer and activator of transcription 5b which mediates the proliferation of normal human B lymphocytes

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