Cellular immune response in convalescents from Ixodes tick-borne borreliosis

Cover Page

Cite item


Ixodes tick-borne borreliosis is a natural focal transmissive infectious multi-system disease featured with complex pathogenesis, which multiple aspects remain unclarified. The persistence stage during this infection associated with prolonged Borrelia presence in metastatic foci and repeated multiple dissemination is most complicated for clinical practice. It is assumed that the chronic process can be caused by an inadequate immune response associated with activated autoimmune mechanisms leading to emergence of permanent irreversible (degenerative and atrophic) changes in affected organs. Patients who experienced tick-borne borreliosis need dynamic observation for assessing disease prognosis providing a maintenance therapy. The purpose of the study was to evaluate an opportunity of using cellular immunity indices for predicting disease transition to a chronic course.

Materials and methods. The study was carried out at the Medical Association of the Far East Branch of the Russian Academy of Sciences. Case report form data, serum and blood plasma samples collected from 22 patients aged 29–83 years old were examined. Immunological examination data from patients with ixodes tick-borne borreliosis (12–18 months after the onset of acute period) were analyzed. Specific IgM and IgG against Borrelia burgdorferi were determined by using the OMNICS diagnostic test system (St. Petersburg). Lymphocyte immunophenotyping was performed on BD FACSCalibur flow cytometer (Becton Dickinson, USA) by using doublelabeled monoclonal antibodies (Beckman Coulter, France).

Results. A variability of activated peripheral blood lymphocytes was found in patients with tick-borne borreliosis evidencing about individual immune response. An imbalanced cellular immune response recorded in seronegative convalescents from tick-borne borreliosis, may be an indirect finding of ongoing Borrelia infection. Finding of specific serum IgG and IgM antibodies in convalescents at late stage coupled to impaired immune system is a warning sign presuming a risk to developing autoimmune reactions. Detection of specific IgM antibodies at late timepoint combined with increased immune cytotoxic potential may be referred to a marker of possible disease transition to chronic course.

About the authors

T. S. Zaporozhets

Somov Institute of Epidemiology and Microbiology

Author for correspondence.
Email: niiem_vl@mail.ru
ORCID iD: 0000-0002-8879-8496

Tatiyana S. Zaporozhets, PhD, MD (Medicine), Senior Researcher, Deputy Director for the Science

690087, Vladivostok, Selskaya str., 1.

Phone: +7 (423) 244-24-34. Fax: +7 (423) 244-14-38.

Russian Federation

S. A. Sokotun

Pacific State Medical University

Email: sokotun.s@mail.ru

PhD (Medicine), Assistant Professor, Department of Infectious Diseases


Russian Federation

A. I. Simakova

Pacific State Medical University

Email: anna-inf@yandex.ru

PhD, MD (Medicine), Professor, Head of the Department of Infectious Diseases


Russian Federation

E. V. Persiyanova

Somov Institute of Epidemiology and Microbiology; Medical Department of Far East Branch of the Russian Academy of Sciences

Email: helen-pers@yandex.ru

PhD (Biology), Senior Researcher; Head of Laboratory of Innovative Medical and Biological Research and Technologies


Russian Federation


  1. Бараулина А.С., Кологривова Е.Н., Жукова О.Б., Чечина О.Е. Особенности продукции цитокинов при хронизации иксодового клещевого боррелиоза // Бюллетень сибирской медицины. 2010. Т. 9, № 1. С. 21–25.
  2. Лукашова Л.В., Карпова М.Р., Лепехин А.В., Пирогова Н.П., Жукова Н.Г., Киюцина Т.А., Добкина М.Н. Иксодовые клещевые боррелиозы // Бюллетень сибирской медицины. 2006. Т. 5, № 1. С. 59–66.
  3. Миноранская Н.С. Патогенетические и иммунологические особенности течения иксодовых клещевых боррелиозов // Сибирский медицинский журнал (Иркутск). 2007. Т. 68, № 1. С. 5–9.
  4. Мошкова Д.Ю., Авдеева М.Г. Клинико-иммунологические особенности воспалительного процесса при клещевом боррелиозе // Эпидемиология и инфекционные болезни. 2016. Т. 21, № 2. С. 86–92. doi: 10.18821/1560-9529-2016-21-2-86-92
  5. Berardi V.P., Weeks K.E., Steere A.C. Serodiagnosis of early Lyme disease: analysis of IgM and IgG antibody responses by using an antibody-capture enzyme immunoassay. J. Infect. Dis., 1988, vol. 158, no. 4, pp. 754–760.
  6. Brunner M., Sigal L.H. Use of serum immune complexes in a new test that accurately confirms early Lyme disease and active infection with Borrelia burgdorferi. J. Clin. Microbiol., 2001, vol. 39, no. 9, pp. 3213–3221. doi: 10.1128/JCM.39.9.3213-3221.2001
  7. Dattwyler R.J., Thomas J.A., Benach J.L., Golightly M.G. Cellular immune response in Lyme disease: the response to mitogens, live Borrelia burgdorferi, NK cell function and lymphocyte subsets. Zentralbl. Bakteriol. Mikrobiol. Hyg. A., 1986, vol. 263, no. 1–2, pp. 151–159.
  8. Jarefors S., Janefjord C.K., Forsberg P., Jenmalm M.C., Ekerfelt C. Decreased up-regulation of the interleukin-12Rβ2-chain and interferon-γ secretion and increased number of forkhead box P3-expressing cells in patients with a history of chronic Lyme borreliosis compared with asymptomatic Borrelia-exposed individuals. Clin. Exp. Immunol., 2007, vol. 147, no. 1, pp. 18–27. doi: 10.1111/j.1365-2249.2006.03245.x
  9. Kinjo Y., Tupin E., Wu D., Fujio M., Garcia-Navarro R., Benhnia M.R., Zajonc D.M., Ben-Menachem G., Ainge G.D., Painter G.F., Khurana A., Hoebe K., Behar S.M., Beutler B., Wilson I.A., Tsuji M., Sellati T.J., Wong C.H., Kronenberg M. Natural killer T cells recognize diacylglycerol antigens from pathogenic bacteria. Nat. Immunol., 2006, vol. 7, no. 9, pp. 978–986. doi: 10.1038/ni1380
  10. Lantos P.M. Chronic Lyme disease // Infect. Dis. Clin. North. Am., 2015, vol. 29, no. 2, pp. 325–340. doi: 10.1016/j.idc.2015.02.006
  11. Lopez-Vergès S., Milush J.M., Pandey S., York V.A., Arakawa-Hoyt J., Pircher H., Norris P.J., Nixon D.F., Lanier L. CD57 defines a functionally distinct population of mature NK cells in the human CD56dimCD16+ NK-cell subset. Blood, 2010, vol. 116, no. 19, pp. 3865–3874. doi: 10.1182/blood-2010-04-282301
  12. Moffat C.M., Sigal L.H., Steere A.C., Freeman D.H., Dwyer J.M. Cellular immune findings in Lyme disease correlation with serum IgM and disease activity. Am. J. Med., 1984, vol. 77, no. 4, pp. 625–632. doi: 10.1016/0002-9343(84)90352-8
  13. Sigal L.H. Immunologic mechanisms in Lyme neuroborreliosis: the potential role of autoimmunity and antigen mimicry. Semin. Neurol., 1997, vol. 17, no. 1, pp. 63–68. doi: 10.1055/s-2008-1040915
  14. Wu L., Van K.L. Natural killer T cells and autoimmune disease. Curr. Mol. Med., 2009, vol. 9, no. 1, pp. 4–14. doi: 10.2174/156652409787314534

Supplementary files

There are no supplementary files to display.

Copyright (c) 2020 Zaporozhets T.S., Sokotun S.A., Simakova A.I., Persiyanova E.V.

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.

СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: серия ПИ № ФС 77 - 64788 от 02.02.2016.

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies