Literature DB >> 8173554

Antigens of Lyme disease of spirochaete Borrelia burgdorferi inhibits antigen or mitogen-induced lymphocyte proliferation.

J W Chiao1, C Pavia, M Riley, W Altmann-Lasekan, M Abolhassani, K Liegner, A Mittelman.   

Abstract

Modulation of cellular immune responses by the spirochaete Borrelia burgdorferi, the bacteria that causes Lyme disease, was demonstrated. When cultured in the presence of sonicated Borrelia preparation (Bb), the mitogen- or antigen-stimulated proliferative responses of normal lymphocytes were consistently lowered. Bb caused the greatest reduction in Concanavalin A (ConA) or antigen-stimulated proliferation, where almost 100% reduction in proliferation could be achieved. Bb also reduced phytohemagglutinin-M (PHA) or pokeweed mitogen (PWM)-stimulated peripheral blood lymphocyte (PBL) proliferation, with the PWM proliferation being the least affected. This regulatory activity was not due to toxicity and was determined to be caused by Bb protein antigens. The degree of the proliferation reduction was directly proportional to both Bb quantity and length of exposure to lymphocytes. IL-2 production was significantly reduced from Bb-exposed lymphocytes. The entry of lymphocytes into the proliferating phases of the cell cycle was also shown to be blocked. These results have demonstrated an immune suppressive mechanism of B. burgdorferi. The magnitude of host immune responses may be dependent on the degree of suppression which is related to the spirochaete quantity and their length of presence in the host.

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Year:  1994        PMID: 8173554     DOI: 10.1111/j.1574-695X.1994.tb00437.x

Source DB:  PubMed          Journal:  FEMS Immunol Med Microbiol        ISSN: 0928-8244


  8 in total

Review 1.  Host-pathogen interactions in the immunopathogenesis of Lyme disease.

Authors:  L T Hu; M S Klempner
Journal:  J Clin Immunol       Date:  1997-09       Impact factor: 8.317

2.  Immunological differentiation between tickborne encephalitis with and without concomitant neuroborreliosis.

Authors:  J Tomazic; A Ihan; F Strle; J Cimperman; J Stare; M Maticic; B Zakotnik
Journal:  Eur J Clin Microbiol Infect Dis       Date:  1997-12       Impact factor: 3.267

3.  Borrelia burgdorferi stimulates the production of interleukin-10 in peripheral blood mononuclear cells from uninfected humans and rhesus monkeys.

Authors:  G H Giambartolomei; V A Dennis; M T Philipp
Journal:  Infect Immun       Date:  1998-06       Impact factor: 3.441

4.  Decreased interleukin-4 and increased gamma interferon production by peripheral blood mononuclear cells of patients with Lyme borreliosis.

Authors:  J Oksi; J Savolainen; J Pène; J Bòusquet; P Laippala; M K Viljanen
Journal:  Infect Immun       Date:  1996-09       Impact factor: 3.441

Review 5.  Lyme Disease Frontiers: Reconciling Borrelia Biology and Clinical Conundrums.

Authors:  Vladimir V Bamm; Jordan T Ko; Iain L Mainprize; Victoria P Sanderson; Melanie K B Wills
Journal:  Pathogens       Date:  2019-12-16

6.  Acute lyme disease IgG N-linked glycans contrast the canonical inflammatory signature.

Authors:  Benjamin Samuel Haslund-Gourley; Stéphane Grauzam; Anand S Mehta; Brian Wigdahl; Mary Ann Comunale
Journal:  Front Immunol       Date:  2022-08-05       Impact factor: 8.786

7.  Assessing the Need for Multiplex and Multifunctional Tick-Borne Disease Test in Routine Clinical Laboratory Samples from Lyme Disease and Febrile Patients with a History of a Tick Bite.

Authors:  Kunal Garg; T Sakari Jokiranta; Sanna Filén; Leona Gilbert
Journal:  Trop Med Infect Dis       Date:  2021-03-17

8.  Evaluating polymicrobial immune responses in patients suffering from tick-borne diseases.

Authors:  Kunal Garg; Leena Meriläinen; Ole Franz; Heidi Pirttinen; Marco Quevedo-Diaz; Stephen Croucher; Leona Gilbert
Journal:  Sci Rep       Date:  2018-10-29       Impact factor: 4.379

  8 in total

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