Autoimmune disorders in patients with granulomatosis diseases after COVID-19: T- and B-cells subsets function

Sarcoidosis and tuberculosis are both granulomatous diseases that have many similarities, making the differential diagnosis of sarcoidosis and tuberculosis difficult, as well as leading to inappropriate treatment selection of both diseases. Autoimmune inflammation (AI) is one of the processes identified tuberculosis and sarcoidosis. Current evidences about the risk and clinical outcomes of COVID-19 infection in patient with sarcoidosis and M. tuberculosis co-infection are still not well understood. SARS-CoV-2 has direct damage to the epithelial cells of the respiratory system, and in-directly due to circulatory disorders. Materials and methods. In the study we analyzed characteristics of autoimmune response in patients with granulomatosis diseases (tuberculosis and sarcoidosis) after COVID-19. We have analyzed articles for the period of December 2019 to March 2023, published in international database (“Medline”, “PubMed”, “Scopus”). The keywords we used “COVID-19”, “SARS-CoV-2”, “tuberculosis”, “sarcoidosis”, “granulomatosis diseases”, “T cells”, “B cells”, “Treg”, “follicular Treg” and “Treg subsets”. The narrative review was carried out in accordance with the PRISMA protocol (http://www.prisma-statement.org) used for this type of study (ID-423604). Results. The influence of COVID-19 infection can also make a significant contribution to the violation of the T- and B-cell immune response, the violation of the nature of cellular metabolism, which will affect the course of granulomatous inflammation in various ways. According to the different researches, autoimmune inflammation can be an important protective mechanism in sarcoidosis and, at the same time, exacerbates the course of tuberculosis infection with the disease progression and pathogen drug resistance formation subsequently. The study of immune response features in patients with COVID-19 showed the presence of several similar characteristics in cellular components of the immune response. Conclusion. Evidence of the presence of autoimmune inflammation in patients with these granulomatous lung diseases, the development of patient immunotypes, including the transferred COVID-19, will be a significant contribution to the development of personalized patient management tactics, taking into account the identified violations of the immune response mechanisms.

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Publication Details

Journal
Russian Journal of Infection and Immunity
Published
2024-08-05
DOI
https://doi.org/10.15789/2220-7619-eou-16874
Primary Topic
COVID-19 Clinical Research Studies
Type
article
Field-Weighted Citation Impact
0.00

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article

Autoimmune disorders in patients with granulomatosis diseases after COVID-19: T- and B-cells subsets function

D.А. Kudlаy, Анна Старшинова, Hong Ling, Miaoqing Zhuang et al.
Russian Journal of Infection and Immunity
COVID-19 Clinical Research Studies
article

Autoimmune disorders in patients with granulomatosis diseases after COVID-19: T- and B-cells subsets function

D.А. Kudlаy, Анна Старшинова, Hong Ling, Miaoqing Zhuang, Irina Dovgaluk, Artem Rubinstein, Anna Malkova, A. Yu. Starshinova, I. V. Kudryavtsev
article en

Abstract

Sarcoidosis and tuberculosis are both granulomatous diseases that have many similarities, making the differential diagnosis of sarcoidosis and tuberculosis difficult, as well as leading to inappropriate treatment selection of both diseases. Autoimmune inflammation (AI) is one of the processes identified tuberculosis and sarcoidosis. Current evidences about the risk and clinical outcomes of COVID-19 infection in patient with sarcoidosis and M. tuberculosis co-infection are still not well understood. SARS-CoV-2 has direct damage to the epithelial cells of the respiratory system, and in-directly due to circulatory disorders. Materials and methods. In the study we analyzed characteristics of autoimmune response in patients with granulomatosis diseases (tuberculosis and sarcoidosis) after COVID-19. We have analyzed articles for the period of December 2019 to March 2023, published in international database (“Medline”, “PubMed”, “Scopus”). The keywords we used “COVID-19”, “SARS-CoV-2”, “tuberculosis”, “sarcoidosis”, “granulomatosis diseases”, “T cells”, “B cells”, “Treg”, “follicular Treg” and “Treg subsets”. The narrative review was carried out in accordance with the PRISMA protocol (http://www.prisma-statement.org) used for this type of study (ID-423604). Results. The influence of COVID-19 infection can also make a significant contribution to the violation of the T- and B-cell immune response, the violation of the nature of cellular metabolism, which will affect the course of granulomatous inflammation in various ways. According to the different researches, autoimmune inflammation can be an important protective mechanism in sarcoidosis and, at the same time, exacerbates the course of tuberculosis infection with the disease progression and pathogen drug resistance formation subsequently. The study of immune response features in patients with COVID-19 showed the presence of several similar characteristics in cellular components of the immune response. Conclusion. Evidence of the presence of autoimmune inflammation in patients with these granulomatous lung diseases, the development of patient immunotypes, including the transferred COVID-19, will be a significant contribution to the development of personalized patient management tactics, taking into account the identified violations of the immune response mechanisms.

Russian Journal of Infection and ImmunityVol. 14(2)
Harbin Medical University (CN), St Petersburg University (RU), Sechenov University (RU), Federal Almazov North-West Medical Research Centre (RU), Institute of Immunology and Physiology (RU), Saint-Petersburg Research Institute of Phthisiopulmonology (RU), Ariel University (IL), Saint Petersburg State Pediatric Medical University (RU)
Ministry of Science and Higher Education of the Russian Federation
Good health and well-being
Openalex Percentile: Top 84%
COVID-19 Clinical Research Studies
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